Microbio final

secondary response

-A much more rapid, and larger, production of antibodies to a pathogen when it infects the body again. -repeat invaders generally are eliminated before they cause noticeable harm , vaccination takes advantage of this -when memory b cells become activated, some will quickly differentiate to form plasma cells which results in the rapid production of antibodies (often IgG or IgA due to class switching)

antigens

-antigen describes any molecule that reacts specifically with an antibody and does not necessarily imply that the molecule can induce a immune response -most antigens are T-dependent antigens meaning that the responding B cell requires a signal from a Th cell -T-independent antigens can activate B cells without Th help and include lipopolysaccharide (LPS) and molecules with identical repeating subunits such as some carbs -antigens differ in effectiveness in stimulating an immune response. proteins generally induce a strong response and lipids and nucleic acids often do not

Lymphatic system

-collection of tissues and organs that bring populations of B cells and T cells into contact with antigens

diveristy of lymphocytes

-gene rearrangement -imprecise joining (during gene rearangement) -combinatorial associations

damaging effects of inflamation

-some enzymes and toxic products in phagocytic cells can damage tissues when released -if inflammation is limited such as from a cut finger, the damage is usually minimal. -if inflammation occurs in a delicate system like the brian and spinal cord membranes then there can be severe life threatening consequences.

Humoral Immunity

-when a naive B cell becomes activated and multiplies, some of the descendents differentiate to become plasma cells (effector B cells -plasma cells make Y-shaped proteins called antibodies which bind to the surfaces of cells toxins viruses and other antigens and so protect the body against it -antibody has two functional regions: the two identical arms and the single stem of the Y-shaped molecule. the ends of the arms attach to antigens and by binding, can neutralize their effects

macrophage

type of phagocytic cell that resides in tissues and has multiple roles, including scavenging debris and producing pro-inflammatory cytokines

leukocytes

white blood cells and important for host defenses 3 types 1. granulocytes 2. mononuclear phagocytes 3. lymphocytes

clonal selection

The process by which an antigen selectively binds to and activates only those lymphocytes bearing receptors specific for the antigen. The selected lymphocytes proliferate and differentiate into a clone of effector cells and a clone of memory cells specific for the stimulating antigen.

what is herd immunity

When a majority of a population are vaccinated against a disease. This means that even people who have not been vaccinated are less likely to get it because there are fewer people to catch it from.

antibody

Y-shaped protein that

lymphocytes

a group of whit eblood cells (leukocytes) involved in adative immunity; B cells and T cells are examples

inflammation

a localized physical condition in which part of the body becomes reddened, swollen, hot, and often painful, especially as a reaction to injury or infection. occurs when microbes are introduced into normally sterile body sites or when tissues are damaged

host cells "self" cells

adaptive immune response can destroy these as well if they are infected with a vrisu or other invader

adaptive immunity

also prevents idseases from recurring (immunological memory) and produces a strong response to re-exposure

antibodies

bind to antigen to target them for destruction or removal by other host defenses

Hematopoeisis

blood cell formation

dendritic cell

cell type responsible for activating naive t cells.

opsonization

coating antigen with antibody enhances phagocytosis

membrane attack complex (MAC)

complement system components assembled to form pores in membranes of invading cells

inflammatory response

coordinated innate response with the purpose of containing a site of damage, localizing the response, eliminating the invader, and restoring tissue function

effector lymphocyte

differentiated descendent of an activated lymphocyte; it has properties that allow itto help eliminate antigen

Tc Cell

effector form of a cytotoxic T cell; it induces apoptosis in infected or cancerous "self" cells

platelets

fragments of megakaryocytes and important for blood clotting

humorla immunity

immunity involving B cells and an antibody response

cell-mediated immunity (CMI)

immunity involving a T-cell response

molecular specificity

part of adaptive immune response where the recognition of antigens is precise

tolerance

part of adaptive immunity where the immune system has the ability to ignore any given molecule -differentiating from what is a dangerous pathogen and what isnt -this is important or else the body would turn against the bodies own cells and attack them like it does invading microbes as well as regularly attack harmless substances such as pollen -pollen allergy, gluten intolerance

clonal selection

process in which a lymphocytes antigen receptor binds to an antigen allowing the lymphocyte to multiply

apoptosis

programmed death of "self" cells that does not cause inflammation

pattern recognition receptiors (PRR's)

proteins on or in cells that recognize specific compounds unique to microbes or tissue damage

cytokines

proteins that function as chemical messengers, allowing cells involved in host defenses to communicate

erythrocytes

red blood cells, transport O2 in the blood

pattern recognition receptors (RR"s) that monitor a cells surroundings

sentinel cells can have PRR;s on cell surface which allows cells to detect invaders in the surrounding environment -toll-like receptors (TLR's), each recognizes a distinct compound or group of compounds associated with microbes. can detect components of outermost layers of microbial cells including lipopolysaccharides, lipoproteins, and flagellin -C-type lectin receptors (CLS's) bind to certain carbohydrate molecules found on the surface of microogranisms

MHS molecules, major histocompatibility complex molecules

1. MHC class I -present endogenous antigens 2.MHC class 2 -present exogenous antigens (taken up) -all nucleated cells produce MHC class 1 molecules but only specialized cell types like dendritic cells, b cells and macrophages (antigen-presenting cells APC's ) make MHC class II molecules

the process of phagocytosis

1. chemotaxis -cells are recrited tot he infection site or damage site by chemoattractants which include products of microorganisms, phospholipids released by injured host cells, chemokines and complement system component C5a 2. recognition and attachment -receptors are used to bind to invading microbes diretly and indirectly -directly, when a phagocytes receptors bind mannose -indirect binding, when a particle has first been opsonized, opsonins tag particles for phagocytosis and have C3b 3. engulfment -sends out pseudopods that surround and elgulf the material. brings material into the cell enclosed in a phagosome 4. phagosome maturation and phagolysosome formations -initially phagosomes don't have antimicrobial capabilities but It can mature to develop things such as more acidity. if the TLR (toll like receptors) indicate a phagosome contains microbial components. eventually phagosome fuses with enzyme-filled lysosomes forming phagolysosome 5. destruction and digestion -different factors work together to destroy an engulfed invader such as -O2 consumption increases dramatically, respiratory burst -enzyme produces reactive oxygen species (ROS) which are toxis -production of nitric oxide, reacts with ROS to produce more toxic compounds -special pumps move protons into phagolysosome which lower pH -enzymes from lysosomes degrade peptidoglycan and other components -antimicrobial peptides damage membranes of invader -lactoferrin binds iron 6. exocytosis -phagolysosome releases undigested debris to outside of cell by fusing with phagocytes cytoplasmic membrane

chapter 14 summary

14.1 Overview of the Innate Immune Defenses First-line defenses prevent entry into the body, sensor systems detect invasion, and effector mechanisms destroy and remove invaders (figure 14.1). 14.2 First-Line Defenses (figure 14.2) Physical Barriers The skin is composed of two main layers—the dermis and the epidermis. Mucous membranes are constantly bathed with mucus and other secretions that help wash microbes from the surfaces (figure 14.3). Antimicrobial Substances Lysozyme, peroxidases, lactoferrin, and antimicrobial peptides inhibit or kill microorganisms (figure 14.4). Normal Microbiota (Flora) Members of the normal microbiota competitively exclude pathogens and stimulate the host defenses. 14.3 The Cells of the Immune System (figure 14.5, table 14.1) Granulocytes Granulocytes include neutrophils, basophils, and eosinophils. Mononuclear Phagocytes Monocytes circulate in blood; macrophages are in tissues (figure 14.6). Dendritic Cells Dendritic cells develop from monocytes; some have other origins. Lymphocytes Lymphocytes, which include B cells, T cells, and innate lymphoid cells (ILCs), are involved in adaptive immunity. 14.4 Cell Communication Surface Receptors Surface receptors bind ligands, allowing the cell to detect substances. Cytokines (table 14.2) Cytokines include chemokines, colony-stimulating factors (CSFs), interferons (IFNs), interleukins (ILs), and tumor necrosis factor (TNF). Adhesion Molecules Adhesion molecules allow cells to adhere to other cells. 14.5 Pattern Recognition Receptors (PRRs) (figure 14.7) Pattern recognition receptors (PRRs) are sensors that allow the body's cells to "see" signs of microbial invasion. Many PRRs detect microbe-associated molecular patterns (MAMPs), and some detect damage-associated molecular patterns (DAMPs). The outcome of certain diseases is influenced by PRR-generated signals from sentinel cells and infected cells. Pattern Recognition Receptors (PRRs) That Monitor a Cell's Surroundings Some toll-like receptors (TLRs) are anchored in the cytoplasmic membranes of sentinel cells such as phagocytes and cells that line blood vessels (figure 14.8). These TLRs detect certain microbial surface components. Membrane-anchored C-type lectin receptors (CLRs) detect certain carbohydrates molecules found on the surface of some microbial cells. Pattern Recognition Receptors (PRRs) That Monitor Material Ingested by a Cell Some toll-like receptors (TLRs) are anchored in endosomal and phagosomal membranes. These TLRs typically recognize characteristics of microbial nucleic acid. Pattern Recognition Receptors (PRRs) That Monitor a Cell's Cytoplasm RIG-like receptors (RLRs) detect viral RNA in a cell's cytoplasm. NOD-like receptors (NLRs) detect microbial components or signs page 384of damage in a cell's cytoplasm (figure 14.9). Certain NLRs in macrophages and dendritic cells allow formation of an inflammasome. An Outcome of Cytoplasmic Pattern Recognition: The Interferon Response Virally infected cells respond by making interferons, causing nearby cells to prepare to undergo apoptosis if they become infected with a virus (figure 14.10). 14.6 The Complement System Complement System Activation The complement system detects microbial cells and antibodies bound to antigens, and is activated in response (figure 14.11). Effector Functions of the Complement System The major protective outcomes of complement system activation include opsonization, an inflammatory response, and lysis of foreign cells (figure 14.12). Regulation of the Complement System Complement regulatory proteins prevent host cell surfaces from activating the complement system via the alternative pathway (figure 14.13). 14.7 Phagocytosis The Process of Phagocytosis (figure 14.14) The steps of phagocytosis include chemotaxis, recognition and attachment, engulfment, phagosome maturation and phagolysosome formation, destruction and digestion, and exocytosis. Characteristics of Macrophages Macrophages are always present in tissues to some extent but can call in reinforcements when needed. A macrophage can become an activated macrophage. Macrophages, giant cells, and T cells form granulomas that wall off and retain material that cannot be destroyed. Macrophages are important sentinel cells. Characteristics of Neutrophils Neutrophils are the first cell type recruited from the bloodstream to the site of damage. 14.8 The Inflammatory Response Swelling, redness, heat, and pain are the signs of inflammation, the body's attempt to contain a site of damage, localize the response, eliminate the invader, and restore tissue function. Factors That Trigger an Inflammatory Response Inflammation is initiated when microbes are detected by pattern recognition receptors (PRRs) or the complement system, or when tissue damage occurs. The Inflammatory Process The inflammatory process results in dilation of small blood vessels, leakage of fluids from those vessels, and movement of leukocytes from the bloodstream into the tissues (figure 14.15). Acute inflammation is characterized by an abundance of neutrophils; chronic inflammation is characterized by macrophage and giant cell accumulation, and granuloma formation. Damaging Effects of Inflammation The inflammatory response can be damaging to the host, and in some cases this is life-threatening. Cell Death and the Inflammatory Response Apoptosis is a mechanism of eliminating "self" cells without triggering an inflammatory response; pyroptosis triggers an inflammatory response. 14.9 Fever Fever results when macrophages release certain pro-inflammatory cytokines. It inhibits the growth of many pathogens and increases the rate of various body defenses.

capter 15 summary

15.1 Overview of the Adaptive Immune Response (figure 15.1) As a result of the primary response to an antigen, the secondary response is more effective. Humoral immunity works to eliminate extracellular antigens; it involves B cells (B lymphocytes). Cell-mediated immunity (CMI) deals with intracellular antigens; it involves T cells (T lymphocytes). Naive lymphocytes cannot respond until they receive signals to become activated. An activated lymphocyte can proliferate, giving rise to effector lymphocytes and memory lymphocytes. Humoral Immunity In response to extracellular antigens, B cells proliferate and then differentiate into plasma cells that function as antibody-producing factories. Memory B cells are also formed. Cell-Mediated Immunity In response to intracellular antigens, cytotoxic T cells proliferate and then differentiate into TC cells that induce apoptosis in "self" cells harboring the intruder. Memory cytotoxic T cells are also formed. Helper T cells proliferate and then differentiate to form TH cells that help orchestrate the various responses of humoral and cell-mediated immunity. Memory helper T cells are also formed. 15.2 Anatomy of the Lymphatic System (figure 15.3) Lymphatic Vessels Lymph, which contains antigens that have entered tissues, flows in the lymphatic vessels to the lymph nodes (figure 15.4). Secondary Lymphoid Organs Secondary lymphoid organs are the sites at which lymphocytes gather to contact antigens. Primary Lymphoid Organs Primary lymphoid organs are the sites where B cells and T cells mature. 15.3 The Nature of Antigens Antigens are molecules that react specifically with an antibody or lymphocyte. The immune response is directed to epitopes (antigenic determinants) on the antigen (figure 15.6). 15.4 The Nature of Antibodies Structure and Properties of Antibodies (figure 15.7) Antibodies have a Y shape with an antigen-binding site at the end of each arm. The tail of the Y is the Fc region. The antibody monomer is composed of two identical heavy chains and two identical light chains. The variable region contains the antigen-binding site; the constant region encompasses the entire Fc region as well as part of the Fab regions. Protective Outcomes of Antibody-Antigen Binding (figure 15.8) Antibody-antigen binding results in neutralization, opsonization, complement activation, immobilization and prevention of adherence, cross-linking, and antibody-dependent cellular cytotoxicity (ADCC). page 413 Immunoglobulin Classes (table 15.1) The five major antibody classes—IgM, IgG, IgA, IgD, and IgE— each have distinct functions. 15.5 Clonal Selection and Expansion of Lymphocytes When an antigen enters a secondary lymphoid organ, only the lymphocytes that specifically recognize that antigen via their antigen receptor will respond (figure 15.10). Lymphocytes may be immature, naive, activated, effector, or memory cells. 15.6 The B-Cell Response: Humoral Immunity Most antigens are T-dependent antigens, meaning the B cells that recognize them require help from TH cells. B-Cell Activation B cells present peptides from T-dependent antigens to TH cells for inspection. If a TH cell recognizes a peptide, it delivers cytokines to the B cell, initiating the process of clonal expansion, which ultimately gives rise to plasma cells that produce antibodies (figure 15.11). Characteristics of the Primary Response In the primary response, the expanding B-cell population undergoes affinity maturation. Under the direction of TH cells, class switching and memory cell formation also occur (figures 15.14, 15.15). Characteristics of the Secondary Response Memory cells are responsible for the swift and effective secondary response, eliminating invaders before they cause noticeable harm (figure 15.12). The Response to T-Independent Antigens T-independent antigens include polysaccharides that have multiple identical evenly spaced epitopes, and LPS (figure 15.16). 15.7 The T-Cell Response: Cell-Mediated Immunity General Characteristics of T Cells (table 15.2, figure 15.19) Cytotoxic (CD8) T cells recognize antigen presented on major histocompatibility complex (MHC) class I molecules. Helper (CD4) T cells recognize antigen presented on MHC class II molecules. Activation of T Cells (figure 15.20) Dendritic cells sample material in tissues and then travel to secondary lymphoid organs to present antigens to naive T cells. The dendritic cells that detect molecules associated with danger produce co- stimulatory molecules and are able to activate both subsets of T cells. Effector Functions of TC (CD8) Cells TC cells induce apoptosis in cells that present peptides they recognize on MHC class I molecules; they also produce cytokines that increase the level of surveillance (figure 15.21). All nucleated cells present peptides from endogenous proteins in the groove of MHC class I molecules. Effector Functions of TH (CD4) Cells (figures 15.11, 15.22) TH cells activate cells that present peptides they recognize on MHC class II molecules; various cytokines are released, depending on the subset of the responding TH cell. Macrophages and B cells present peptides from exogenous proteins in the groove of MHC class II molecules. Subsets of TH cells direct the immune system to an appropriate response for a given antigen. 15.8 Natural Killer (NK) Cells NK cells mediate antibody-dependent cellular cytotoxicity (ADCC). NK cells also induce apoptosis in host cells that are not bearing MHC class I molecules on their surface (figure 15.23). 15.9 Lymphocyte Development Generation of Diversity Mechanisms used to generate the diversity of antigen specificity in lymphocytes include rearrangement of gene segments, imprecise joining of those segments, and combinatorial associations of heavy and light chains (figure 15.25). Negative Selection of Self-Reactive B Cells Negative selection occurs as B cells develop in the bone marrow; if the B-cell receptor of a developing B cell binds material in the bone marrow, that B cell undergoes apoptosis. Positive and Negative Selection of Self-Reactive T Cells Positive selection permits only those T cells that show moderate recognition of the MHC molecules to develop further. Negative selection also occurs.

Dendritic cells expressing co-stimulatory molecules activate T cells that recognize the presented antigen. TC (CD8) cells recognize antigen presented on MHC class I molecules; they induce apoptosis in target cells and produce cytokines that increase the level of surveillance. TH (CD4) cells recognize antigen presented on MHC class II molecules (found on B cells and macrophages); they activate the target cells and secrete various cytokines that orchestrate the immune response.

18. Name three types of antigen-presenting cells. -dendritic cells, macrophages, b cells, all use MHC class II 19.If an effector CD8 cell recognizes antigen presented on an MHC class I molecule, how should it respond? -CD8 is another way to say cytotoxic T cells (Tc). CD8 molecules are the receptors tc cells used to recognize cells that are presenting antigen bearng MHC class 1 molecules. Tc cells that are presented with MHC class 1 antigens are encountering cells that have become infected and they -first will deliver apoptotic signal to infected cell -release cytokines that up-regulate other immune cells telling them to be more vigilant 20.Why would a person who has AIDS be more susceptible to the bacterium that causes tuberculosis? -reaction to the bacterium that causes tuberculosis mycobacterium tuberculosis is Tcell dependent -HIC/AIDS destroys Th cells thus cripling the activating arm of t-cell dependent immune response causing thee bacteria to grow largely unchecked

Microassessment The adaptive immune response is directed against epitopes on antigens.

7.How is an epitope different from an antigen? 8.Would a denatured antigen be expected to have the same epitopes as its native (undenatured) counterpart?

complement system

A series of proteins that circulate in the blood and the fluid that bathes the tissues these proteins typically circulate in an inactive form but presence of microbial invaders start a reaction cascade that activates the system -each major complement system protein splits into two fragments as well C3, C3a, C3b

antigen

substance that causes an immune response, body creates antibodies to learn substance that causes the body to produce antibodies

Phagocytosis

the engulfing and digesting of material including invading microbes

regulation of complement system

Complement regulatory proteins prevent host cell surfaces from activating the complement system via the alternative pathway, molecules in host cell membranes can bind to regulatory proteins that quickly inactivate C3b which prevents host cells from being opsonisized

lymphocyes

the pain participants in adaptive immunity will recognize microbial invaders or foreign material and when it does, they will begin to proliferate (multiple) which allows the most effective lymphocytes to eliminate a specific invader when encountered

two basic strategies of adaptive immune response

Humoral immunity -the eliminating of microbial invaders as well as their toxins from the bloodstream and tissue fluids (extracellular antigens because they're not in a host cell) -involves B cells (B lymphocytes, develops in the bone marrow in mammals) Cell-Mediated immunity (CMI) -cellular immunity -deals with invaders in a host cell -invaders are intracellular antigens and include viruses and bacteria that replicate in a hot cell -cell-mediated response also attacks cancerous cells -involves T cells (t lymphocytes) that mature in the thymus

surface receptors

"eyes" and "ears" of cell, Usually span membrane, connect outside to inside, Binding to specific ligand induces response

B cell

-Each B cell is programmed to make a single specific antibody so when an antigen is introduced, only the B cells capable of making the antibodies that bind to the antigen begin multiplying which creates a population of clones (copies of the specific B cells capable of making appropriate antibodies)

effector functions of Th (CD4) cells

-Th cells orchestrate immune responses by activating B cells and macrophages and direct the activities of B cells, macrophages and T cells -Th cells recognize antigens on MHC class II molecules (which are typically only found on antigen-presenting cells lik b cells and macrophages) which gather process and present exogenous material so when a Th cells recognizes one of these peptides, it delivers cytokines to activate the cell

B-cell receptor (BCR)

-This is why naive B cells know to respond -this is a membrane-bound version of the antibody the B cells is genetically rpogrammed to make so that whhen a naive B-cell encounters a antigen that its BCR binds to, the interactions signals the cell that it should response -before it can begin to muiltiply, it needs a second signal that confirms that the antigen needs to be eliminates -The BCR must bind to antigen ,that receives confirmation from T cell then that specific B cell becomes activated and begins multiplying

lymphocytes

responsible for adaptive immunity - B and T cells, participate in adaptive responses. found in lymphoid organs (lymph nodes, spleen, appendix, tonsils, thymus, bone marrow) and in blood. very specific in antigen recognition. usually in lymph nodes and other lymphatic tissues -innate lymphoid cells (such as NK cells), lack specificity in antigen recognition that B and T cells have. common near mucous membranes NK cells, a type of ILC, kills certain types of cells

inflammatory process

sequence of events that result in the filation of small blood vessels leakage of fluids from those blood vessels, and migration of leukocytes out of the bloodstream and into the tissues -greater blood flow occurs when the diameter of blood vessels increase because of inflammatory mediators which is what causes the ehat and redness associated with inflammation. will slow down blood flow to capillaries allowing more fluid to leake from vessels and intot he tissue which includes transferrin, complment system proteins, and antibodies. the increase of fluids in tissue causes swelling and pain that comes with inflammation as well as a direct effect of certain chemicals on snesory nerve endings

complement system

series of proteins in blood and tissue fluids that can be activated to help destroy and remove invading microbes

primary response and secondary response

the first adaptive response to a particular antigen, as a result of this encounter, the immune system will remember the mechanism that was effective against that specific antigen so if the antigen is encounteres again later in life, a stronger antigen-specific adaptive immune response will occur (secondary response)

immunogenic

the relative ability of an antigen to elicit an immune response -small molecules are usually not immunogenic

helper T cell

type of lymphocyte programmed to activate B cells and macrophages and assist other parts of the adaptive immune system

cytotoxic T cell

type of lymphocyte programmed to destroy infected or cancerous self cells

B cell

type of lymphocyte programmed to make antibodies

subsets Of T cells (cell-mediated immunity)

Cytotoxic T cells -responsible for destroying host cells that contain viruses or are otherwise "corrupt" -after it is activated, it proliferates and some of its descendants become Tc cells or (TCL, cytotoxic T lymphocyte) that when it encounters an infected self cell it instructs the cell to undergo apoptosis and by sacrificing it, it prevents the intracellular invader from muiltply. some may multiply and become memory cytotoxic cells Helper T cells -responsible for directing and assisting the various responses of humoral and cell-mediated immunity -after it is activated, it will proliferate and some descendents differentiate to become an effector form called a Th cell which produce specific cytokines that activate B cells and macrophages and may also produce cytokines that direct and support other cells of the immune system including other T cells. -some of the descendants of the activated helper T cells become memory helper T cells -look the same but differ in their surface proteins CD markers Regulatory T cells -similar to other T cells but have TCR's but instead of fostering an immune response they prevent one -stops immune system from overreacting and fostering an immune response, prevents an immune response Treg T cell receptor -every T cell has this surface moleucle -binds a specific antigen -functionally similar to B-cell but TCR does not recognize antigen that is free in fluids, antigen but be presented by one of the bodies own cells

primary response

The first response of the immune system when exposed to an antigen. -takes about 10 to 14 days for a significant concentration of antibodies to accumulate -during this delay, a person might experience signs and symptoms of an infection, the immune system system is actively responding -naive B cells will get the signal from Th cells and then they multiply, generating a population of cells that recognize the antigen -some of the activated b cells continue dividng while other differentiate to form antibody-secreting plasma cells -each plasma cell will undergo apoptosis but activated b cells continue multiplying and differentiating which increase numbers of plasma cells as long as an antigen is present resulting in a slow but steady increase of antibody molecules -during the primary response, proliferating B cells will undergo affinity maturation which is when spontaneous mutations occur in certain regions of the antibody genes causing slight changes to antigen-binding sites -during the primary response b cells also undergo class switching which is when some activated B cells differentiate into plasma cells that secrete other antibody classes instead of differentiating into plasma cells that secrete IgM. -B cells in lymph nodes usually switch to IgG production and those in MALT (Muscosal associated lymphoid tissue) switch to IgA production providing mucosal immunity -after class switiching some b cells beome memory b cells as persist in the body for year and accumulate in high enough numbers to give fast secondary responses if the same antigen is encountered again later

ligand

a molecule that can bind to a given receptor. -when a ligand binds to a surface receptor, the internal part of the receptor is modified which triggers a specific response by the cell

adaptive immunity

a specialize ddefense system that develops throughout life as a result of exposure to microbes to certan other types of foreign material and increases the host's ability to defend itself

adhesion molecules

allow cells to adhere to other cells 1.chemokines are found in various cells and are trigger chemotaxis 2,.. colony stimulating factors (CSF's) are found in various cells and stimulate growth and differentiation of diferent kinds of leukocytes 3. interferons are found in various cell and regulate immune response, antiviral 4. interleukins IL's, -IL-1 found in macrophages and epithelial cells and trigger T-cell activation, macrophage activation, and induces fever -IL-2 are found in t cells and trigger t-cell proliferation -IL-4 is found in t-cells and mast cells and promote antibody reponses IL-6 is found in T-lymphocytes and macrophages and trigger T and B cell growth, inflammatory reponse, and fevers 5. Tumor Necrosis Factor (TNF) are found in macrophages, T cells , and NK cells and promote inflammation, cytotoxic for some tumor cells, and regulates certain immune functions

extent of inflammation

depends on nature of injury but is a localized reponse that begind immediartely upon injury and increases rapidly. acute inflammation, short-term inflammatory response, abundance of neutrophils. when infection is under control, neutriphils stop entering and macrophages clean up by ingesting dead cells and debris. then new capillaries grow, destroyed tissues are replacesd, and scar tissue forms chromic inflammation, when the bodys defenses cannot limit the infection. can last for years, macrophages and giant cells accumulate and granulomas form

clonal selection steps

development -immature B cellls: as these develop, a funtionally limitless assortment of b-cell receptors is randomly generated -naive B cells- each cell is programmed to reocognize a specific epitope on an antigen; B-cell receptors guide that recognition activation -activated B cells can proliferate because their b-cell receptors are bound to antigen X and the cells have received required signals from Th cells proliferation and differentiation -plasma cells (effector B cells) are desendants of activated B cells and secrete large quantities of antibody molecules that bind to antigen X -memory b cells are long-lived desendants of activates B cells that recognize antigen X when it is encountered again effector action -antibodies, these neutralize the invader and tag it for destruction

antigen exposure

each time the body is exposed to an antigen the adaptive defense system will first learn then remember the most effective response to that antigen

plasma cell

effector form of a B cell; it functions as an antibody-secretung factory

Th cell

effector form of a helpter T cell; it activates B cells and macrophages, and releases cytokines that stimulate other cells of the immune system

factors that trigger an inflammatory response

inflammation triggers such as detection of MAMP's (microbe associated molecular pattern) and DAMP's(damage associated molecular pattern) triggers host cells to release inflammatory mediators (pro inflammatory cytokines and chemicals like histamines) inflammatory inducers -microbes, when PRR's detect MAMP's, the cells produce inflammtory mediators. TNF induces the liver to synthesize acutephase proteins which are a group of proteins that facilitate phagocytosis and complment activation. microbial surfaces trigger complement activation which leads to an inflammatory response -tissue damage, sensors of DAMP's involve NOD like recepptors (NLR's) so when the cells detect DAMP's they release inflammatory mediators. if blood vessels are injured, two enzymatic cascades are activated, the coagulation cascade (blood clotting) and production of molecules that increase blood vessel permeability

Memory lymphocytes

long-live descendents of activated lymphocytes that can quickly respond when a spectific antigen is encountered again

neutrophil

major type of phagocytic cell in blood; neutrophils quickly move to infected tissues, where they destroy invading microbes

antigen

molecule that reacts specifically with either an antibody or an antigen receptor or a lymphocyte

innate immuntiy

present at birth and is germ-line encoded( from one generation to the next and includes anatomical barriers as well as certain cell types and chemicals

adaptive immunity

protection provided by host defenses that develop throughout life; involves B cells and T cells when lymphocytes identify and destroy microbial invaders and other foreign material

adaptive immunity

protection provided by immune responses that improve due to exposure to antigens; involved B cells and T cells

NK cells

Natural killer cells are innate lymphoid cells (ILC's) which are lymphocytes lacking antigenic specific receptors that characterize b and t cells -NK cells assit adaptive immune response -NK cells induce apoptosis in antibody-bound "self" cells -NK cells destroy host cells that have viral or other foreign proteins inserted into their membrane , they can do this because htey have Fc receptors for IgG molecules on their surface (Fc receptors bind the red flag part of antibody molecules) -NK cells then attach antibodies and delivers perforina nd protease containing ganuels directly to antibody bound cells initiating apoptosis

structures and properties of antibodies (immunoglobulins)

-Y shaped proteins with two general pats, the arms and the stem -the two identical arms are called Fab regions and have ends that bind to antigens -the stem is the Fc region -all antibodies have the same basic Y structure called an antibody monomer and consists of two copies of a high-molecular weight polypeptide chain called the heavy chain and two copies of a lower-molecular-weight polypeptide chain called the light cain -light chains have 2domains (when amino acids fold into chains, they have characteristic domains -most heavy chains have 4 domains -variable region is the portion at the ends of the Fab regions and accounts for the antigen-binding specficity of the antibody and part of this region is the antigen-binding site which is the portion that attaches to a specific epitope -constant region includes entire FC region as well as part of the two Fab regions -5 general types of constant regions that corresond to the major classes (also called isotypes) of immunoglobulin (Ig) molecules IgM, IgG, IgA, IgD, IgE each class has distinct functions and properties

adaptive immune response is highly regulated

-a naive lymphocytes (has not encountered antigen previously) cannot react until it receives specific signal to confirm that the antigen is a microbe is a microbe or other harmful substance -an activated lymphocyte can proliferate so that every single naive lymphocyte becomes activated -some of the descendants of activated lymphocytes that multiply are effector lymphocytes which are short-lived cells that express specific traits that help eliminate invader -the rest of the descendents become memory lymphocytes which are long-lived cells that can be activated more quickly if the antigen is encountered again, memory cells are responsible for the effectiveness of the secondary response

effector functions of the complement system

-activation of complement system leads to 3 major protective outcomes 1.opsonization, C3b concentration increases when complement system is activated and these molecule will bind to bacterial cells.,has 2 effects -continued complement activation via an alternative pathway and opsonization -opsonized material is easier for phagocytes to bind to and engulf because phagocytes have receptors that attach specifially to opsonina such as C3b 2. inflammatory response, C5A is a chemoattractant that draws pahgocytes to where the complment system was activated. C3a and C5b induce changes in endothelial cells ining blood vells contibuting to vascular permeability that coems with inflammation. also cause mast cells to release pro-inflammatory cytokines 3. lysis of foreign cells, complexes of complement system proteins (C5b, C6 C7 C8 and multiple C9's), will assemble in cell membranes forming donut shaped structures called membrane attack complexes (MAC's) which creates pores in the membrane causing cells to lyse. dont affect gram-positive bacteria because of the thick peptidoglycan layer of these cells prevent the complment system components from reaching cytoplasmic membranes

Lymphatic Vessels

-carry lymph that is derived from tissue fluid -forms from circulatory system as blood enters capillaries some liquid is forced out to join tissue fluid (extracellular fluid bathing tissues) -most of the liquid will re-enter the capillaries but some is left in the tissues, the excess fluid joins lymphatic vessels and passes through lymph npdes and empties back into the blood circulatory stsem -inflammatory response causes more fluid to enter the tissues at the site of inflammation causing an increase in the antigen contianing fluids that enter lymphatic vessels

pattern recognition receptors (PRR's)

-allow the cells to see signs of microbial invasion, if it is detected, the cell will produce cytokines to alert other components of the defense system -many detect components of certain groups of microbes such as peptidoglycan, teichoic acid, lipopolysaccharide, and lipoproteins, flagellin subunits, and microbial nucleic acid (microbe-associated molecular patterns MAMPs') or PAMPS (pathogen associated molecular patterns) but are not exclusive to pathogens so MAMPS is preferred -some recognize damage-associated molecular patterns (DAMP's) which are molecules that indicate host cell dmaage ex. a macrophage's PRR detects bacterial products, pro-inflammatory cytokines are produce, inflammatory response produce. -if a dendritic cell detects bacterial products then the information is relayed to lymphocytes and they mount an immune response. if virally infected PRR's detect viral nucleic acid, that cell produces an interferon whcih alerts immune cells to the presence of a virus and promotes an antiviral response in nearby tissue -PRR's are located in 3 distinct locations 1. on cell surface 2. in endosomes and phagosomes 3. free in cytoplasm

pattern recognition receptors (PRR's) that monitor a cells' cytoplasm

-allows cells to monitor own cytoplasmic contents for signs of invasion 1.RIG-like receptors (RLR's) are cyrto[;asmic proteins that detect viral DNA. found in most cell types. can distinguish viral RNA rom normal RNA because its usually double stranded and lacks a cap 2. NOD like receptors (NLR's) are cytoplasmic proteins that detect either microbial components or signs of cell damage and are found in most cell types but are important in macrophages and dendiritc cells. microbial products most detectes are peptidoglycan, flagellin, components of secretion system some pathogenic bacteria use to inject molecules into host cells inflammasome a structure formed when NLR's in macrophages and dendritic cells detect invasion and combine with other proteins in he cytoplasm. this structure triggers inflammation by activatin pro-inflmmatory cytokine

primary lymphoid organs

-bone marrow and thymus -bone marrow is where hematopoietic stem cells reside (give rise to all blood cells) -B and T cells originate in bone marrow -B cells mature in the bone marrow -T cells migrate to the thymus and mature there -once mature, the lymphocytes will gather in secondary lymphoid organs waiting to encounter antigens

Response to T-Independent Antigens

-can activate B cells without the aid of Th cells -relatively few are T-independent -pT independent antigens are significant because they are not immunogenic in young children which is why children younger than 2 ore more susceptible to pathogens like haemophilus influenzae and streptococcus pneumoniae which coat themselves in polysaccharide capsules -there are vaccines made from purified capsules but they do not stimulate an immune response in young children

pattern recognition receptors (PRR's) that monitor material ingested by a cell

-can inspect material ingested by cell -specific toll-like receptors face lumen of organelle (inside of organelle exposed to organelles contents) -can recognize nucleic acids that indicate microbial origin becuase some nucleotide sequences are more commin in bacterial DNA than host cell DNA<,RNA's viruses are often double stranded during the replication cycles, DNA viruses may generate long dsRNA since both strands are usually used for transcription

granulocytes

-contain cytoplasmic granules filled with compounds important for protective function -neutrophils, basophils, eosinophils -neutrophils- Phagocytosis; they also release substances that trap and destroy microbial invaders. Most abundant leukocyte in blood. granules don't stain well -eosinophils, release chemicals that destroy eukaryotic parasites found mainly in tissues below mucous membranes. important in removing parasitic worms. involved in causing some symptoms of allergies and removing other. granules stain red with eosin -basophil, release histamine and other inflammation inducing chemicals. found in blood involved in allergic reactions and inflammation. granules stain dark purple with methylene blue. contian histamine and other chemicals that increase capillary permeability during inflammation. mast cells are similar in appearance and function but are found in tissues rather than blood and involved in many allergic reactions

activation of T cells

-dendritic cells are scouts of innate immunity -immature dendritic cells are in peripheral tissues like skin and mucosa gathering materials using phagocytosis and pinocytosis -dendritic cells also have tentacle like extensions to aid in gathering material from those areas -dendritic cells also have TLR's or toll like receptors and other receptors that allow them to recognize pathogens, and if they do, they will begib to take up more material then enter lymphatic vessels to transport them to secondary lymphoid organs to encounter naive T cells -these dendtritic cells mature, dendritic cells that detected invading microbes will begin to produce surface proteins called co-stimulatory molecules which are like emergency lights that interact with the T cell -naive t cells recognize the antigens presented by dendiritc cells become activated -t cells that recognize antigens presented by dendiritc cells that do not have emergency lights will become anergic (unresponsive) and will undergo apoptosis -dendritic cells cross-present antigens, can present peptides for both MHC class I molecules and MHC class II molecules and so can activate both cytotoxic t cells as well -once the t cell sia activated it can undergo clonal selection and expansion and eventually form effector cells and memory cells which then leave lymphoid organs and circulate in the blood stream. they can also enter tissues at sites of infection -Th1 cells promote a response effective against intracellular invaders -Th2 cells promote a response effective against parasitic worms -Th17 cells promote a response against extracellular invaders

fever

-important host defense and a strong indication of infectious disease especially abacterial one - goes from about 37 degrees to 37.8 degrees -this occurs when macrophages release pro-inflammatory cytokines in response to microbial products. cytokines act as messages carried in the bloodstream to the brain where the temperature-regulating center raises the body temperature in response -moderate fevers enhance several protective processes such as inflammatory response, phagocytic activity, multiplication of lymphocytes, release of substances attracting neutrophils, and production of interferons and antibodies. release of leukocytes into the blood from bone marrow also increases -fever-inducing cytokines and other substances are pyrogens. pyrogenic cytokines are endogenous proteins meaning the body makes then whereas microbial products such as lipopolysaccharide (LPS) are exogenous pyrogens meaning they are introduced from external sources

cell death and the inflammatory response

-in addition to necrosis (cell death from tissue damage) host cells can self-destruct to allow host to eliminate cells that are no lnger needed and can sacrifice "self" cells that can spread an infection -apoptosis, is a programmed cell death that does not trigger an inflammatory response. -pyroptosis is a programmed self-destruction that triggers an inflammatory response

Effector functions of Tc (CD8) cells

-induce apoptosis in infected "self" cells can destroy cancerous "self" cells -regular and cancerous cells are distinguished due to antigen presentation on MHC class I amolecules because all nucleated cells routinely degrade part of the proteins they produce which results in peptides in the groove of MHC class I molecules wich go to the cell surface for inspecting -"self" cells will produce normal proteins and shouldnt be recognized by any Tc cells -if the self cell is infected with a replicating virus or microorganism, then the peptides from the invading microbe will be presented on the MHC class I molecules making it a target for lethal efector functions of T cells which also occurs if the self cell is prpducing abnormal proteins that characterize cance r cells

mononuclear phagocytes

-monocytes, phagocytosis. found in blood. they differentiate into either macrophages or dendritic cells when they migrate into tissues. circulate and blood -macrophages, phagocytosis, important type of sentinel cell. found in tissues, sometimes known by different names based on the tissue where they are found, differentiated form of monocytes and are present in nearly all tissues especially the liver spleen lymph nodes lungs and peritoneal (abdominal) cavity. -dendritic cells, collect antigens from tissues then bring them to lumphocytes that gather in the secondary lymphoid organs (lymph nodes, spleen, appendix, tonsils) and an important type of sentinel cell. sentinel cell that functions as a scout. enguld material in the tissues then bring it to cells of adaptive immune system for inspection. most develop from monocytes.

B cell activation

-naive B cells gather in secondayr lymphoid organs where there are antigens, their antigen receptop (b cell receptor) will bind to t-dependent antigen and tages in the antigen with endocytosis -the antigen is then degraded into peptide ragments delieverd to protein structures called MHC class II molecules which move to b cell surgace where they present the antigen pieces for more inspection by Th cells -antigen presentation is when Th cells gather in the secondary lymphoid organs and scan the naive b cells that are presenting antigens if one of the T cell receptors (Th cells antigen receptor) binds one of the peptide fragments being presented by a b cell then the b cell is activated by the T cell by delivering cytokines to the B cell which initiates the process of clonal expansion for that B cell -if no Th cells recognize the peptibes presented then the B cell may become anergic or unresponsive to future exposure of the antigen which results in tolerance to that antigen which is how the adaptive imune system avoids responses against "self" and other harmless antigens

T cells

-never produce antibodies like b cells -effector T cells directly interact with target cells to cause changes -like b cells they have multiple copies of a receptor on their surface that recognizes a specific epitope -T-cell receptor (TCR) has two polypeptide chains with a variable and constant region each, like an arm of a b cell receptor

characteristics of neutrophils

-quickly moves into an area of trouble and ready to eliminate invaders -first cell type at the site of damage from the bloodstream -more killing power than macrophages but have a relatively short life span of only a few dats -kill microbes through pahocytosis and canrelease contents of their granules (act like mobile grenades) exploding in an area of destructive enzymes and antimicrobial peptides -releases their DNA to form NET's (neutrophile extracellular traps) which ensnare microbes allowing granule contents in teh NET to destroy them

secondary lymphoid rgans

-sites where antigens have entered the body and brought into contact with dense populations of lymphocytes -lymph nodes, spleen, tonsils -lymph nodes capture materials from lymphatics -spleen collects materials from blood -secondary lymphoid are places for immune system cells to interact and transfer cytokines, this is the only place where adaptive immune responses can be initiated -peyer's patches are tissues in the intestinal wall that inspect samples of intestinal contents and present it to lymphocytes. -peyers patches are part of a network of lymphoid tissues called mucosa-associated lymphoid tissue (MALT) which is important in mucosal immunit -mucosal immunity is the immune response that revents microbed from invading the body through mucous membranes -lymphoid tissues under the skin are skin-associated lymphoid tissue (SALT)

cytokines

-voices f the cell -binding of a cytokine to its receptor induces a change in the cell such as growth, differentiation, movement, or cell death 1. chemokines. allow immune cells to sense the location where they are needed such as an are of inflammation 2. colony-stimulating factors,(CSF's) important in the multiplication and differentiation of leukocyes. when more are needed during an immune response, a variety of different colony-stimulating factors direct immature cells into the appropriate maturation pathways 3. interferons (IFN's), discovered due to antiviral effects but are important in regulatory mechanisms by stimulating responses of some cells and inhibiting others 4. interleukins (IL's)m produced by leukocytes and have diverse often overlapping functions and as a group are important in both innate and adaptive immunity 5. tumor necrosis factor (TNF), discovered due to its role in killing tumor cells but also helps intiiate inflammtory response and triggers apoptosis groups of cytokines act together. pro-finlammatory cytokines (TNF, IL-1, IL-6, and others) contribute to inflammation other promote antibody response and some stimulate certain types of t-cells

outcome of cytoplasmic pattern recognition: interferon response.

-when a cells PRR's detect viral viral RNA, the cell will synthesize and secrete an interferon (IFN) that induces nearby cells to develop an antiviral state. -interferon molecles attack to specifi receptors on neighboring cells causing them to express suicide enzymes, (iAVP's) which can be activated by viral dsRNA and when activated by dsRNA(usually only foudn in virally infected cells) causing the infected ones to be sacrificed when cells bind interferon. uninfected cells remain functional but can undergo apoptosis if infected

characteristics of macrophages

1) always present in tissue 2) live for weeks to months 3) retain killing power by continually regenerating lysosomes 4) continually replaced by circulating monocytes (monocyte migration increases in response to invasion & tissue damage) -can develop into activated macrophages if surrounding cells produce certain cytokines or other hcemicals -if activated macrophages fial to destroy icrobes, the phagocytes can fuse together to form giant cells. macrophages, giant cells and T clels form concentrated froups called granulomas that retain organisms and other material that cannot be destroyed preventing them from escaping and infecting other cells but can also harm host because it interferes with normal tissue function -have good PRR"s letting them see microbes in the surrounding environment, in ingested material, and in cytoplasm

characteristics of t cells

1. Cytotoxic/ CD8, -antigen recognition: peptides presented on MHC class I molecules -effector form: Tc cell -potential target cells: all nucleated cells - effector function: induces target cell to undergo apoptosis -source of antigen recognized by effector cell, endogenous (produced in target cell) 2. Helper/CD4 -antigen recognition, peptides presented on MHC class II moelcules -effector form, Th cell -potential target cells, B cells, macrophages -effector function, activates target cell -source of antigen recognized by effector cell: exogenous (produced outside target cell) -antigen must be presented by another host cell, t cell receptor does not interact with free antigen -host cell does this by partly degrading antigens then displaying individual peptides -peptides are are cradled in groove of proteins called MHS molecules, major histocompatibility complex molecules, like a hot dog bun holding a hot dog -cytotoxic and helpter T cells are identical microscopically so scientists distinguish them based on presence of surface proteins called CD marker, cluster of differentiation -most cytotoxic T cells have CD8 marker and called CD* T cells and most helper T cells have CD4 marker and called CD4 T cells -CD4 is a HIV receptor

immunoglobulin classes

1. IgM -first antibody class produced during immune response -principal class produced in response to T-independent antigens -provides direct protection by neutralizing viruses and toxins, immobilizing motile origins, preventing microbes from adhering to cell surfaces, and cross-linking antigens -binding of IgM to antigen leads to activation of the complement system (classical pathway) 2. IgG -most abundant class in the blood and tissue fluids -provides longest-term protection because of long half-life -provides direct protection by neutralizing viruses and toxins, immobilizing motile organisms, and preventing microbes from adhering to cell surfaces, and cross-linking antigens -binding of IgG to antigen facilitates phagocytosis, leads to activation of the complment system (classical pathway) and allows antibody-dependent cellular cytotoxicity -transported across the placenta, providing protection to a developing fetus; long half-life extends the protection through the first several months after birth 3. IgA -most abundant class produced but the majority of it is secreted into mucus, tears, and saliva providing mucosal immunity -protects mucous membranes by neutralizing viruses and toxins, immobilizing motile organisms, and preventing attachment of microbes to cell surfaces -component of breast milk; protects the intestinal tract of breast-fed infants 4. IgD -involved in the development and maturation of the antibody response -it functions in blood not well understood 5. IgE -binds via the Fc region to mast cells and basophils -bound IgE allows those cells to detect parasites and other antigens and respond by releasing their granule contents -involved in many allergic reactions

first line defenses

1. first line defenses -prevent microbes and other foreign material from entering the bodies tissues -skin, mucous membranes, antimicrobial substances and normal microbiota on these surfaces -sentinel cells are certain host cells that serve as lookouts at certain locations to detect certain components such as peptidoglycan, pattern recognition receptors which are sometimes located on sentinel cells -complement system, may become activated in response to certain stimuli which will set off a chain reaction that will remove and destroy invadine microbes -interferon (IFN) is produces when a host cell recognizes that it is infected by a virus and so it warns nearby cells about the virus, they can also shut off themselves (the cell) to prevent the virus from replicating -phagocytes go tot he site of infection and they specialize in phagocytosis, process of engulfing and digesting microbes -inflammatory response, a coordinated response that results when various sensory systems detect infection or tissue damage -fever, an innate response which is when body temperature goes higher than normal and it interferes with pathogen growth and enhance effectiveness of other responses

defense systems

1. first line defenses prevent microbial acitivty and are like security walls -skin and mucous membranes -antimicrobial substances 2. sensor systems detect invader and are like security cameras -pattern recognition receptors -complement system 3. innate effector actions eliminate threats and are like security teams -interferon response -phagocytosis -complement activation -inflammatory response -fever

MC ch 14

1. lysozome does what -found in secretions like mucus, saliva, tears, and human milk. -it hydrolyzed peptidoglycan 2. the hematopoeitic stem cells in bone marrow can develop into which of the following 1) RBC 2) T cell 3) B cell 4) monocyte 5) macrophage -all 5 of them 3. all of the following refer to the same type of cell except (macrophage, neutrophil, poly, and PMN) -macrophage 4. considering the role of pattern recognition receptors (PRR's) which are they least likely to detect? (peptidoglycan, glycolysis enzymes, lipopolysaccharides, flagellin, certain nucleotide sequences) -glycolysis enzymes 5. the direct and immediate action of interferon on a cell is to -stimulate synthesis of inactive suicide enzymes 6. a pathogen that can avoid the complement component C3b would directly protect itself from -opsonization 7. which of the following statements about phagocytosis is false. a)Phagocytes move toward an area of infection by chemotaxis. b)Digestion of invaders occurs within a phagolysosome. c)Phagocytes have receptors that recognize C3b bound to bacteria. d)Phagocytes have receptors that recognize antibodies bound to bacteria. e)Macrophages die after phagocytizing bacteria, but neutrophils regenerate their lysosomes and survive. -E, macrophages die after phagocytizing bacteria but neutrophils regenerate lysosomes and survive 8. If you are analyzing the cell types in a granuloma, which of the following are you least likely to find? a)Neutrophils b)Macrophages c)Giant cells d)T cells -neutrophils 9.All of the following trigger an inflammatory response except a)engagement of PRRs. b)complement system activation. c)interferon induction of antiviral protein synthesis. d)tissue damage. -interferon induction of antiviral protein synthesis which is a protective immune response 10.Which of the following statements about inflammation is false? a)Vasodilation results in leakage of blood components. b)The process can damage host tissue. c)Neutrophils are the first to migrate to a site of inflammation. d)Apoptosis induces inflammation. e)The signs of inflammation are redness, swelling, heat, and pain -apoptosis induces inflammation

protective outcomes of antibody-antigen binding, depend partly on antibody class

1. neutralization -toxins and viruses must bind specific molecules on a cell surface before they can damage that cell while a toxin or virus coated with antibodies cannot attach to cells and is said to be neutralized 2. Opsonization -phagocytic cells have receptors for the Fc region of IgG molecules making it easier for the phagocyte to engulf antibody coated antigens 3. complement system activation -antigen-antibody complexes (immune complexes) can trigger the classical pathway of complement system activation -when multiple molecules of certain antibody classes are bound to a cell surface, a specific complment initiation of an inflammatory response and formation of membrane attach complexes 4. immobilization and prevention of adherence -binding of antibodies to flagella interferes with a microbes ability to move; binding to pili prevents a bacterium from attaching to the surfaces -movement and attachment are often necessary for a pathogen to infect a host so antibodies that flagella or pili can prevent infection 5. cross-linking -ends of the two arms of an antibody can bind separate but identical antigen molecules , linking them. the overall effect is that large antigen-antibody complexes form creating big mouthfuls of antigens fir phagocytic cells to engulf 6. antibody-dependent cellular cytotoxicity (ADCC) -when multiple IgG molecules bind to a virally infected cell or a tumor cell, that cell becomes target for destructiong by natural killer (NK) cells -the NK cell attaches to the Fc regions of IgG and once attached, kills the target cell by delivering destructive compounds directly to it

short answer ch 14

1.Describe how the skin protects against infection. -skin and mucous membranes are physical barriers or mechanical factors which prevent pathogens and other foreign particles from entering. secretions of the skin also allow growth of certain normal microiota that prevent growth of pathogenic microbes. drya dn slightly acidic conditions of the skin does not favor microbial growth. 2.What factors in saliva aid in protection against microbes? -slightly acidic (6.35- 6.85) -salivary fluid constantly flushes contents of oral cavity continuously toward troat which enter the stomach -lysozyme is bacteriolytic and inhibits bacteria growth -other enzymes such as peroxidase, and lactoferrin found in saliva can interfere with microbial growth -contains antibodies that can readily attack pathogens present in mouth 3.Why is iron availability important in body defenses? -lysozyme and lactoferrin act on microbes preventing them from obtaining iron which is needed for microbial growth. 4.Name two categories of cytokines and give their effects. -interleukins are involved in the activation and proliferation of T cells -colony-stimulating factors stimulate the production of lymphocytes from the bone marrow and also direct immature immune cells into specific pathways when excess WBC's are needed to produce an immune response -interferons attack viruses and cancer cells, inhibit viral replication and engulf them, stimulate production of antibodies form B lymphocytes -tumor necrosis factor inhibits the growth of cancer cells, causes fever during bacterial infection, releases growth factors and stimulates differentiation of lymphocytes 5.What is the function of pattern recognition receptors? -proteins capable of recognizing molecules frequently found in pathogens or molecules released by damaged cells (MAMPs and DAMP's) 6.Contrast the pathways of complement activation. -the complement system consists of circulating proteins that direct antibodies to destroy pathogens. -classical pathway of complement system provides the most rapid and effective activation of cascade mechanisms and is activated by antigen-antibody immune complex -alternative pathway is triggered by the presence of bacteria, viruses and other parasites (antibody mediated) and activate the complement protein 7.How do complement proteins cause foreign cell lysis? -MAC formes pores that disrupt cellular integrity causing cell lysis -this complex formation triggers "phagocytosis" of infectious agent by opsonization mediated by opsonosis which enhances phagocytosis by making the antigen more susceptible to an immune response 8.How do phagocytes enter tissues during an inflammatory response? -squeeze through blood vessels (diapedesis) which is when cells move to the site of inflammation by ameboid movement (squeezing through endothelial cells) 9.How is acute inflammation different from chronic inflammation? -acute inflammation signs are produced suddenly and may last for only a short period of time and is characterized by significant neutrophil count raise -chronic inflammation has inflammation occurring periodically but for a prolonged period. characterized by increased macrophage count and giant cells 10.Describe the function of apoptosis. -apoptosis is programmed cell death -process of cell death removes the overgrown cells maintaining an organ or tissues shape -apoptosis removed damaged or diseased cells as they become toxic if they remain in the body

The complement system can be activated by three different pathways that each lead to opsonization, an inflammatory response, and lysis of foreign cells. Describe the outcome of opsonization. The body's own cells do not trigger the alternative pathway of complement system activation. Explain why this is so. Some pathogens produce C5a peptidase, an enzyme that destroys C5a. How would this benefit the pathogen?

1.Describe the outcome of opsonization. opsosonin is an immune molecule that enhances the process of phagocytosis by making the antigen more susceptible to an immune response 2.The body's own cells do not trigger the alternative pathway of complement system activation. Explain why this is so. -activtion and binding of C3b is an antibody-mediated immune mechanism that only recognizes foreign cells and not body cells 3.Some pathogens produce C5a peptidase, an enzyme that destroys C5a. How would this benefit the pathogen? -this will prevent an immune response. C5 is involved n the complement system and is important for inflammation and cell death

Physical barriers that prevent microbes from entering the body include skin and mucous membranes. Antimicrobial substances, including lysozyme, peroxidase enzymes, lactoferrin, and defensins, are on body surfaces. The normal microbiota excludes pathogens and promotes immune system development.

1.How does peristalsis protect against intestinal infection? -peristalsis is the involuntary rhythmic contraction of smooth muscles of the GI tract which propel food forward -peristaltic movements help prevent intestinal infections in 2 ways 1. moving unabsorbed or undigested food to the rectube from where microbes and digestive waste can be eliminates -propel food at a rhythmic pattern which prevents fermentation and growth of harmful bacteria 2.What is the role of lactoferrin and transferrin? -lactoferrin sequesters free iron and so removes an essential nutrient needed for bacterial growth -transferrin transports and stores iron inhibiting the growth and propagation of microbes 3.How would damage to the ciliated cells of the respiratory tract predispose a person to infection? -cilia constantly beat in an upward motion moving material away from the lungs to the throat where they can be swallowed -damaged to cilia cause the mucocilliary escalatory to work less efficiently or even stop altogether which causes the lungs to be in danger of being invadedsince it cannot remove materials away

Microassment B cells are programmed to make antibodies that help eliminate extracellular antigens. Cytotoxic T cells are programmed to destroy infected "self" cells as a means of eliminating intracellular antigens. Helper T cells are programmed to orchestrate the adaptive immune response. Recognition of antigen by a naive B cell or T cell serves as a signal to that cell that it needs to respond; in order to become activated, however, the cell requires a confirming second signal.

1.How is the cell-mediated response different from the humoral response? 2.Why is it important that B cells and T cells become activated before they can begin multiplying in response to an antigen? 3.How would you expect a TC cell to respond if it encountered a TH cell that was infected with a virus?

First-line defenses prevent microbes from entering tissues. Sensor systems recognize invading microbes. Innate effector actions eliminate the invader.

1.List two sensor systems of the innate defenses. Pattern recognition receptors complement system 2.Describe three innate effector actions. -production of an interferon (IFN): a type of protein that warns nearby cells about the virus; the cells react by preparing to shut down their biosynthetic activities if they become too infected, thereby depriving the virus of a mechanism to replicate-phagocytosis: cells that specialize in engulfing and digesting microbes and cell debris in response to a bacterial infection or tissue damage-fever: a higher than normal body temp; interferes with the growth of some pathogens and can enhance the effectiveness of other responses 3.In addition to peptidoglycan, which molecules unique to bacteria might pattern recognition receptors recognize? -peptidoglycan, lipopolysaccharide

Surface receptors allow a cell to detect molecules present outside that cell. Cytokines provide cells with a mechanism of communication. Adhesion molecules allow one cell to adhere to another.

10.What is a ligand? -surface receptors that span the plasma membrane and connect the outside of the cell to the inside allowing internal workings of cell to sense and respond to external stimuli. each receptor is specific to the compounds that it will bind to. a molecule that can bind to a given receptor is called a ligand for that receptor 11.How do cytokines function? --during infectious conditions, cytokines produce local or system response and in general are released locally and act on nearby cells. can be autocrine or paracrine action. sometimes they can enter systemi circulation and act on other cells (endocrine action) cytokines can be pleiotropic (ct on different cell types) and redundant (stimulates the release of other cytokines that produce similar or overlapping actions) 12.How could colony-stimulating factors be used as a therapy? -CSF are a type of cytokine that can direct the maturation of leukocytes as needed during an immune response and can be used as therapy for the side effects of chemotherapy. CSF's can accelerate the formation of neutrophiles

In response to an antigen, only those lymphocytes that recognize the antigen multiply. Depending on their developmental stage, lymphocytes may be referred to as immature, naive, activated, effector, or memory cells.

12.Describe the clonal selection theory. -each B-cell produces antibodies to one specific antigen epitope. To do this, B-cells undergo the process of clonal selection which creates an array of possible antibodies for the recognition of antigens -clonal selection occurs in primary lymphoid organs where hematopoietic stem cells create a wide variety of immature-B-cells wich create near-infinite possible B-cell receptor shapes which after many trials, the receptor-shapes that recognize self-antigens are destroyed and those that recognize foreign antigens are selected. after passing the selection process, they become naive lymphocytes and will wait until the present antigen binds to the receptor and they become activates 13.How does a naive lymphocyte differ from an activated one? naive lymphocytes -have antigen receptors but have not yet encountered the antigen to which they are programmed to respond activated lymphocytes -able to proliferate, theyr ecognize that a specific antigen is present because their antigen receptor has attached to it and they have receives the second signal confirming the antigen requires a response 14.What would happen if the body lost the ability to make memory lymphocytes? -memory lymphocytes are the lymphocytes that are produced by the body against the antigen during the first infection. these lymphocytes mount a strong immune response when the antigen is reintroduced and helps in better protection against the antigen. if the body lost the ability to make memory lymphocytes, then the immune response wont be fast and strong nd the body will be more prone to foreign antigen Primary and secondary are mediated by B and T cells.a primary response is slower because clonal selection and proliferation takes some time to find a proper antibody and mount a response. The secondary response is faster because an effective antibody already exists in the arsenal, proliferation of the memory cell into activate lymphocytes does not take as long as the clonal selection process

Sentinel cells use pattern recognition receptors (PRRs) to detect microbial components in the surroundings and in ingested material. Many cells use PRRs to determine if they are infected. Viral RNA triggers an interferon response.

13.give three examples of MAMPs. -microbe associated molecular patterns(MAMPS) or pathogen associated molecular patterns (PAMPS) are on microbes -3 examples , peptidoglycans (cell wall components of bacteria), lipopolysaccharides, (specific to gram negative bacteria), and flagellin proteins 14.If a cell produces antiviral proteins (AVPs), what happens to that cell when those proteins encounter long dsRNA? -RIG-like receptors (RLR's) detect viral dna and provide a mechanism for an infected cell to detect the invader. when RLR's detect viral dna (long dsRNA), the cell will synthesize and secrete interferons -interferons attach to specific proteins on the infected cell and neighboring cells causing the cell to produce suicide enzymes that lead to apoptosis. 15.Why would the discovery of TLRs alter the view that innate immunity is non-specific? -patterns associated with TLR's show that some responses may be specific

The binding of a T-dependent antigen to a B cell's receptor is an initial signal to that B cell that an invader is present. Before that B cell can become activated, however, it must get a second signal in the form of cytokines delivered by a TH cell that recognizes the same antigen. Activated B cells proliferate, ultimately becoming either plasma cells that secrete antibody molecules or long-lived memory cells. Affinity maturation and class switching occur in the primary response; these allow a swift and more effective secondary response. B cells that bind to T-independent antigens can become activated without the aid of TH cells.

15.Describe the significance of class switching. -class switching is important for 2 reasons 1. b cells found in mucosal associate lymphoid tissue class wtich to produce IgA antibodies providing the basis of what is called mucosal immunity, first line of defence against microbes in digestive tract 2. B cells in lymph nodes class switch to produce IgG antibodies which allows te antibodies to remain in circulation much longer providing better coverage 16.How does the ability to bind antigen increase as B cells multiply? -affinity maturation, B cells that are better able to bind up antigens are more likely to proliferate. -when a B cell binds to antigen, the Tc cells will interact and provide cytokines to stimulate further maturation and proliferation. the b cells with the best binding will proliferate more and reproduce more efficienty so only the best performing b cells reproduce and antigen binding affinity improves through subsequent generations 17. Why should B cells residing in the mucosa-associated lymphoid tissues produce IgA? -IgA molecules both decrease motility of microbes and prevent viruses and bacteria from attaching to cell surfaces by interfering with their adherens

The process of phagocytosis includes chemotaxis, recognition and attachment, engulfment, phagosome maturation and phagolysosome formation, destruction and digestion, and exocytosis. Macrophages are long-lived and always present in tissues; they can be activated to have more power. Neutrophils are highly active, short-lived phagocytic cells that must be recruited to the site of damage.

19.How does a phagolysosome differ from a phagosome? -phagolysosomes contain enzymes and toxic substances. 20.Tuberculosis is characterized by granulomas called tubercles. What is a granuloma? -giant cells form concentrated groups called granulomas that wall off and contain organisms or other material that cannot be destroyed. as part of the progress of tuberculosis, granulomas known as tubercles form. although the tubercles prevent the microbes from escaping the infect other cells, they harm the host by interfering with normal tissue function 21.What could a microorganism do to avoid engulfment by a phagocyte? -chemically overpower phagocytes and destroy them -destroy C5a a complement protein that attracts phagocytes -could attract complement regulatory proteins that lessen or eliminate effects of opsonization

Natural killer (NK) cells can kill antibody-bound cells by antibody-dependent cellular cytotoxicity (ADCC). NK cells also kill stressed cells that lack MHC class I molecules on their surface

21.What mechanism do NK cells use to kill "self" cells? -when a virus invades a cell, part of its RNA code prevents cell from producing major MHC class I molecules and without these surface molecules, cells cannot be targeted by cytotoxic T cells and thus can potentially proliferate -NK cells can recognize these infected cells and deliver apoptotic signal, killing the cell 22.What can cause a "self" cell to not display MHC class I molecules? -some viruses interfere with the ability to either produce or deploy MHC class I proteins. because of this, cells that are not showing these molecules are likely infected and the removal of these molecules helps the virus evade Tc cells 23.Why might a virus that interferes with the production of the host's MHC class I molecules encode a non-functional version? -cells that do not have MHC class I molecules are killed by NK cells, some viruses interfere with the ability to produce MHC ! molecules while others can create decoy MHC class I molecules and while they cannot be killed by Tc cells, they can be killed by NK cells -decoy MHC class I will slow down recognition by NK cells as well

The inflammatory response is initiated when microbes invade or tissues are damaged. The outcome is dilation of small blood vessels, leakage of fluids from those vessels, and migration of leukocytes out of the bloodstream and into the tissue. Inflammation helps contain an infection, but the response itself can be damaging. Apoptosis destroys "self" cells without initiating inflammation; pyroptosis triggers an inflammatory response.

22.Describe two general events that can initiate inflammation. - when tissue is damaged like when an object penetrates ski -when skin is exposed to irritants 23.Describe two changes in cells undergoing apoptosis. -shape of cell alters, enzymes cut DNA of cell, portions of cell buds out causing cell to shrink -macrophages then engulf and destroy those cells 24.Infection of the fallopian tubes can lead to infertility. Why would this be so? -in inflammation, some enzymes and toxic products in phagocytic cells are released damaging tissues. if infection of the fallopian tubes occurs, the resulting inflammation can lead to scarring abscess formation, and tubal damage, possibly resulting in infertility

Describe two general events that can initiate inflammation. Describe two changes in cells undergoing apoptosis. Infection of the fallopian tubes can lead to infertility. Why would this be so?

25.What is a pyrogen? -pyrogens are circulating proteins that can increase the body temperature above normal levels causing fevers. generally occurs due to presence of pathogens that release pyrogens 26.How does fever inhibit the growth of pathogens? -bacteria typically grow at around normal body temp of 37 degrees and are less likely to cause disease when there is a fever because bacterial growth rates will typically decline above certain optimal levels allowing more time for other defences to destroy invaders -a moderate temperature rise increases rate of enzymatic reactions, enhances inflammatory responses of phagocytic killing by leukocytes, replication of lymphocytes, release of neutrophil-attracting substances, and production of interferons and antibodies 27.Syphilis was once treated by infecting the patient with the parasite that causes malaria, a disease characterized by repeated cycles of fever, shaking, and chills. Why would this treatment control syphilis? -these repeated fevers were observed to kill the spirochete bacteria that causes syphilis

complement system activation

3 different pathways 1. alternative pathway, quickly and easily triggered. triggered when C3b binds to goreign cell surfaces allowing other complment proteins to attach forming C3 convertase 2. Lectin pathway, involved pattern recognition molecules called mannose binding lectins (MBL's) and bind to certain arrangements of multiple mannose molecules, mannose is a carbohydrate found on some microbial cells especially bacteria and fungi 3. classifcal pathway, requires antibodies and when these antibodies bind to an antigen they will form an antigen-antibody complex or an immune complex and will sometimes interact with the same complent system component involved with the elctin pathway to form a C3 convertase

Microassment Lymphatic vessels carry antigen-containing fluid collected from tissues to the lymph nodes. Secondary lymphoid organs are where antigens that have entered the body are brought into contact with dense populations of lymphocytes. Primary lymphoid organs are where T and B cells develop.

4.What is lymph? 5.What are Peyer's patches? 6.How would mucosal immunity prevent diarrheal disease?

Granulocytes include neutrophils, basophils, and eosinophils. Mononuclear phagocytes include monocytes and macrophages. Dendritic cells function as scouts for the adaptive immune system. Lymphocytes are responsible for adaptive immunity.

7.Which type of granulocyte is the most abundant? neutrophils 8How are most dendritic cells related to macrophages? all come from hematopoeitic stem cells found in bone marrow. mononuclear phagocytes or monocytes are always in circulation but when they migrate into issue, they become macrophages or dendritic cells 9.Why can bone marrow transplants be used to replace defective lymphocytes? -hematopoietic stem cells can turn into any lymphocyte

phagocyte

cell type that specializes in engulfing and digesting microbes and cell debris (phagocytosis)

antigen-presenting cells (APCs)

cells such as B cells, macrophages, and dendritic cells that can present exogenous antigens to naive or memory T cells, activating them

first-line defenses

first line defense against invading microbes 1. physical barriers -all exposed surfaces are lined with epithelial cells which are tightly packed tpgether on a basement membranne -slin is difficult for microbes to penetrate since it consits of two later, the dermis and epidermis. dermis contains tightly woven fibrous connective tissue so its tough and durable, episdermis is outermoost later and has many layers of epithelial cells. the outermost sheets are made of dead cells filled with water-repelling protein (keratin). cells continously flake off from here taking microbes adhered to them with it. -mucous membrane sline the digestive, respiratory and genitourinary tracts . most mucous membranes have mechanissm to move microbes towards areas where they can be eliminates such as peristalsis which is the contractions of the intestinal tract which moves food water and microbes out. there is also the respiratory tract that has ciliated cells that beat in an upward motion to move things away from the lungs to the throat 1 billion intestinal cells pero hour are shed 2. antimicrobial -skin and mucous membranes have substances that inhibit or kill microorganiss -salty residue on skin (comes from sweat) evaporates and inhibits all but salt-tolerant microbes -lysozyme degrades peptidoglycan and is found in tears, saliva, and mucus and is also found in phagocytic cells blood, and the fluid that bathes tissues -peroxidases form antimicrobial compounds using hydrogen peroxide (H2O2) and the microogranisms that prodce catalyze are less effective to these. perioxidase systems are found in saliva, milk, body tissues, and phagocytes -lactoferrin is an iron-bidning protein in saliva mucus milk and some types of phagocytes -transferrin is similar to lactogerrin and is found in blood and tissue fluids -antimicrobial peptides (AMP's) are short chains of amino acids that have antimicrobial activity -defensins is a group of AMP's and is important in portecting epithelial borders. theyre positively charged AMP's that insert into microbial membranes forming [pres -defensins are also produced by phagocytes 3. normal microbiota (flora) - population of organisms that routinely grow on the body surfaces of healthy humans -competitive exclusion of pathogens, such as covering binding sites on host cells which blocks pathogens from attaching and can also consume available nutrients -some normal microbiota can produce compounds that are toxic to other bacteria such as cutibacterium which degrades lipids (on the skin), in the GI tract, some e.coli strains synthesize colicins which are toxic to some bacteria, and lactobacillus grows in the vagina and produce s lactic acid which results in an acidic pH that inhibits the grown of some pathogens

hematopoeitic stem cell

found in blood marrow and is the origin of all blood cells -capable of long-term self renewal (can repeatedly divide)

Major Histocompatibility complex (MHC) molecules

host cell surface proteins that present antigen to T cells

innate immunity

host defenses involving anatomical barriers, sensory systems that recognize patterns associated with microbes or tissue damage, phagocytic cells, the inflammatory response and fever

the activities of individual lymphocytes will change as they encounter antiigens

immature lymphocytes -have not fully developed their antigen-specific receptors naive lymphocytes -have antigen receptors but have not yet encountered the antigen to which they are programmed to respond activated lymphocytes -able to proliferate, theyr ecognize that a specific antigen is present because their antigen receptor has attached to it and they have receives the second signal confirming the antigen requires a response effector lymphocytes -descendants of activated lymphocytes that have the ability to produce specific cytokines or other protective substances. plasma cells are effector B cells, Tc cells are effector cytotoxycic T cells, and Th cells are effector helper T cells memory lymphocytes -long lived descendants of activated lymphocytes; they can quickly become activated when an antigen is encountered again. Memory lymphocytes are responsible for the speed and effectiveness of the secondayr response