MICRO EXAM 4

CH15 MULTIPLE CHOICE

" Multiple Choice 1. The variable regions of antibodies are located in the 1. Fc region. 2. Fab region. 3. light chain. 4. heavy chain. 5. light chain and heavy chain. a) 1, 3 b) 1, 5 c) 2, 3 d) 2, 4 e) 2, 5 2. Which of the following statements about antibodies is false? a) If you removed the Fc portion, antibodies would no longer be capable of opsonization. b) If you removed the Fc portion, antibodies would no longer be capable of activating the complement system. c) If you removed an Fab portion, an antibody would no longer be capable of cross-linking antigen. d) If IgG were a pentamer, it would bind antigens more efficiently. e) If IgE had longer half-life, it would protect newborn infants. 3. Which class of antibody can cross the placenta? a) IgA b) IgD c) IgE d) IgG e) IgM 4. A person who has been vaccinated against a disease should have primarily which of these types of serum antibodies against that agent 2 years later? a) IgA b) IgD c) IgE d) IgG e) IgM 5. Which of the following statements about B cells/antibody production is false? a) B cells of a given specificity initially have the potential to make more than one class of antibody. b) In response to antigen, all B cells located close to the antigen begin dividing. c) Each B cell is programmed to make a single specificity of antibody. d) The B-cell receptor allows B cells to detect antigen. e) The cell type that makes and secretes antibody is called a plasma cell. 6. Which term describes the loss of specific heavy chain genes? a) Affinity maturation b) Apoptosis c) Clonal selection d) Class switching 7. Which of the following specifically refers to an effector lymphocyte? a) B cell b) CD8 T cell c) CD4 T cell d) Plasma cell 8. Which markers are found on all nucleated cells? a) MHC class I molecules b) MHC class II molecules c) CD4 d) CD8 9. Which of the following are examples of an antigen-presenting cell (APC)? 1. Macrophage 2. Neutrophil 3. B cell 4. T cell 5. Plasma cell a) 1, 2 b) 1, 3 c) 2, 4 d) 3, 5 e) 1, 2, 3 "

Lymphatic system

- Lymphatic system brings B and T cells into contact with antigens - Blood in the circulatory system enters capillaries. Some fluid is forced out into joints. The Fluid thats forced out enters lymphatic vessels (they carry antigens). This fluid is lymph fluid. - The lymph sends antigens to various places Sites where lymphocytes gather to contact Ag: - Lymph nodes, spleen, tonsils, peyers patches (these secondary lymphoid organs are the only site where the adaptive immune response can be initiated. All places where cells come into contact with antigen)

Peyers patch: Secondary lymphoid organ

- M cells allow molecules/antigens to enter and come into contact with phagocytic cells (dendritic/macrophages). - M cells are dispersed through epithelial cells - Peyers patch is part of a network of tissue called MALT. - T cells and B cells gather, and dendritic cells bind to antigens and introduce them. M cells transfer material from intestinal cells to the Peyer's patches. The dendritic cells grab antigen to present to the lymphocytes. Allows for them to come into closer contact with T and B to initiate an adaptive immune response.

Receptors

- MHC molecule on host cell contains antigen w/ mhc binding site - T cell receptor contains Variable and costant region. Antigen binds to the variable region which is what changes

Affinity maturation: B cell response

- Proliferating B cells undergo changes that improve immune response - B cell that binds to aG the longest is most likely to proliferate - Longer the binding the better

Lymphocyte receptors: T and B cells

- Provide specificity and bind to a specific antigen - Cells binds to a specific pathogen to produce a specific response - Cells can do this because of their receptors. The receptors have a specific binding site that allows them to bind to a specific antigen and create memory.

MHC Classes

- T cells are involved in eliminating antigen - MHC class I molecules present endogenous antigens (anti-gens made within the cell). MHC class II molecules present exogenous antigens (antigens taken up by a cell). - Cytotoxic T cells recognize antigen presented on MHC class I molecules, whereas helper T cells recognize antigen presented on MHC class II molecules.

Humoral Immunity

Immunity involving B cells and an antibody response

create flashcards to learn the 5 classes of globulants

Immunoglobin igG: - most abundant in the blood - transported across the placenta igA: - tears - bodily fluids - breast milk igD: nothing, just know it by name igE

Cell-Mediated Immunity

In response to intracellular antigens, cytotoxic T cells proliferate and then differentiate into TCcells 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 THcells that help orchestrate the various responses of humoral and cell-mediated immunity. Memory helper T cells are also formed.

Characteristics of the Primary Response

In the primary response, the expanding B-cell population under-goes affinity maturation. Under the direction of TH cells, class switching and memory cell formation also occurs

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.

Describe the characteristics and roles of surface receptors, cytokines, and adhesion molecules in innate immunity

Innate immunity: What we're born with and has been passed down through generations. Surface receptor: Membrane proteins that are bind specific to a signaling molecule. Each receptor is specific with respect to the compound or compounds it will bind; a molecule that can bind to a given receptor is called a ligand for that receptor. Ligand binding triggers cell response/effect such as chemotaxis. Cytokines: Signal cells to come to the area and act. Binding of a cytokine to its receptor induces a change in the cell such as growth, differentiation, movement, or cell death. Adhesion molecules: Adhesion molecules on the surface of cells allow those cells to "grab" other cells. For example, when phagocytic cells in the blood are needed in tissues, the endothelial cells that line the blood vessels synthesize adhesion molecules that bind to passing phagocytic cells. This slows the rapidly moving phago-cytes, allowing them to then leave the bloodstream.

Describe each of the different types of leukocytes involved in innate immunity and their respective functions. Which of these leukocytes have phagocytic ability? Which ones are involved in inflammation?

Leukocytes = WBC Neutrophils: - Granulocyte - Most abundant WBC - Polymorphonucleated - Phagocytic "first responder" cell that moves to infected tissue to phagocyte invading microbes - React when there is injury or high stress Eosinophils: - Granulocyte - Red stained granules that contain histamines, cytokines and other biologically active molecular components - Phagocytes but not as efficient as neutrophils. Destroy parasites and react to allergens. - Found in mucous membranes Basophils: - Granulocyte - Least abundant - Bilobed or unilobed - Dark purple stained granules containing histamines - Respond to allergens / involved in inflammation - Found in the blood Lymphocytes - Agranulocyte - Can differentiate into NK, B, or T cells - Large circular nucleus with small cytoplasmic space B and T cells: - Adaptive response - Found in lymphoid organs such as lymph nodes, spleen, appendix, etc. Innate lymphoid cells: - Various roles and locations Monocytes: - Migrate from Blood -> tissue and differentiate into dendritic cells. Become macrophages / phagocytes. - Large, irregular kidney bean shaped nucleus with clear cytoplasmic space Dendritic cells: Sentinel cells that collect antigens from tissue and bring them to lymphocytes gathered in the secondary lymphoid organs. Macrophages: Unrego phagocytosis and found in the tissuee.

Briefly compare and contrast the roles of lymphatic vessels, the various secondary lymphoid organs, and primary lymphoid organs.

Lymphatic vessles: Flow within the lymphatic system occurs via the lymphatic vessels, or lymphatics. - Vessels carry lymph - Fluid is forced out of capilaries and joins tissue fluid and enters lymphatic vessels. - Antigens are carried along with it and become lymph. - Passes through the LV, then the secondary lymphoid organ lymphnodes. Secondary: - Where antigens are brought into contact with lymphocytes - The lymph nodes, spleen, and tonsils. Lymph nodes, for example, capture materials from the lymphatics, and the spleen collects materials from blood. -these organs are the only sites where adaptive immune responses can be initiated. Primary lymphoid organs: bone marrow and thymus. - B cells and T cells - B cells and T cells all originate in the bone marrow but only B cells mature there; immature T cells migrate to the thymus and mature there. - Once matured, the lymphocytes gather in secondary organs to encounter antigens

" Lymphocytes

Lymphocytes, which include B cells, T cells, and innate lymphoid cells (ILCs), are involved in adaptive immunity. - Cells of the immune system

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.

Compare and contrast the roles of macrophages and neutrophils in phagocytosis.

Macrophages: - Resident macrophages reside in tissues - Eat dead cells and debris - Monocytes leave blood and migrate into tissues to become other dentritic cells and phagocytes / macrophages - Long life span (weeks to months) - Agranulocytes Neutrophils: - Respond to areas in trouble - Early stages of inflammation - First cell type recruited to the site of damage from the bloodstream. - They have more killing power than macrophages - Short life span (Few days; once they've used their granules they die) - Granulocyte

Characteristics of the Secondary Response

Memory cells are responsible for the swift and effective secondary response, eliminating invaders before they cause noticeable harm

Lymphocyte Development: " Negative Selection of Self-Reactive B Cells

Negative selection occurs as B cells develop in the bone marrow; cells to which material binds to their B-cell receptor are induced to undergo apoptosis.

Describe the characteristic and roles of granulocytes, mononuclear phagocytes, dendritic cells and lymphocytes

Neutrophils: - Granulocyte - Most abundant WBC - Polymorphonucleated - Phagocytic "first responder" cell that moves to infected tissue to phagocyte invading microbes - React when there is injury or high stress Eosinophils:- Granulocyte - Red stained granules that contain histamines, cytokines and other biologically active molecular components - Phagocytes but not as efficient as neutrophils. Destroy parasites and react to allergens. - Found in mucous membranes Basophils: - Granulocyte - Least abundant - Bilobed or unilobed - Dark purple stained granules containing histamines - Respond to allergens / involved in inflammation - Found in the blood Lymphocytes - Agranulocyte - Can differentiate into NK, B, or T cells - Large circular nucleus with small cytoplasmic space B and T cells: - Adaptive response - Found in lymphoid organs such as lymph nodes, spleen, appendix, etc. Innate lymphoid cells: - Various roles and locations Monocytes: - Migrate from Blood -> tissue and differentiate into dendritic cells. Become macrophages / phagocytes. - Large, irregular kidney bean shaped nucleus with clear cytoplasmic space Dendritic cells: Sentinel cells that collect antigens from tissue and bring them to lymphocytes gathered in the secondary lymphoid organs.

Overview of Granulocytes

Neutrophils: - Phagocytosis - releases substances that trap and destroy microbial invader Basophils: - release histanine and other inflamitory chemicals, mast cells similar but found in tissue Eosinophils: - destroy eukaryotic parasites (parasitic worm helminths) - Mainly in the tissue and mucous membrane - Phagocytic ability

Cells of the immune system have membrane receptors that bind to molecules and lead to certain immune responses. How is a PRR on a cell of the innate immune response (Ch. 14) different from B cell and T cell receptors (Ch. 15)? In your explanation, provide one example for each receptor type to illustrate your description

PRR receptor: PRR receptors are able to recognize any components of the pathogen that may be considered pathogenic. Examples of PAMPS include flagella, LPS, nucleic acids, mannose, peptidoglycan and viruses. PRR receptors are involved in the innate immune response meaning that they are not programmed to react to a specific epitope on an antigen. They simply react to any pathogen that they might come across within the immune system. T and B cell receptors however are programmed to respond to a specific antigen since they are involved in adaptive immunity. Cytoplasmic: Cytoplasmic receptors detect cell damage Phagosome/lysosome: Phagosome/lysosome receptors detect for digested components Surface: Surface receptors monitor the cells surroundings

"Pattern Recognition Receptors (PRRs) "

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. "

Describe the key steps of phagocytosis. How would a pathogen prevent an encounter with phagocytes? How would a pathogen avoid recognition and attachment to a phagocyte?

Phagocytosis: The immune systems way of ridding any foreign invaders that have entered through infection sites / other openings; Defense mechanism that includes digestion. Steps: 1. Chemotaxis: Chemoattractants recruit phagocytes to the infection site. 2. Recognition and attachment: Phagocyte has receptors that recognize: Direct recognition: phagocyte binds to surface of microbe like mannose. Indirect binding: Particle has been opsonized by C3B. C3B binds, then phagocyte binds to c3B. Phagocytes can bind onto opsonized particles easier bc of their specialized receptors. 3. Engulfment: Once attached, the phagocyte sends out pseudopods to surround and engulf. Material is enclosed in a phagosome. 4. Phagosome maturation and phagolysosome formation: pH becomes more acidic and fuses with lysosomes to form a phagolysosome. 5. Destruction and digestion: O2 increases and ROS is produced. pH conditions continue to lower and antimicrobial peptides damage the foreign invader. Lysosomes increase. Chopped into pieces. 6. Exocytosis: Phagolysosome fuses with phagocytes cytoplasmic membrane. Undigested material is expelled. - Avoiding an encounter: capsule or M protein inactivates C3B. M protein and capsule will prevent it from happening. - Avoiding recognition and attachment: Pathogen is bound to the Fc portion, and the pathogen can't bind.

Describe the detailed steps of phagocytosis.

Phagocytosis: The immune systems way of ridding any foreign invaders that have entered through infection sites / other openings; Defense mechanism that includes digestion. Steps: 1. Chemotaxis: Chemosttractants recruit phagocytes to the infection site. 2. Recognition and attachment: Direct recognition: phagocyte binds to surface of microbe like mannose Indirect binding: Particle has been opsonized by C3B. Phagocytes can bind onto opsonized particles easier bc of their specialized receptors. 3. Engulfment: Once attached, the phagocyte sends out pseudopods to surround and engulf. Material is enclosed in a phagosome. 4. Phagosome maturation and phagolysosome formation: pH becomes more acidic and fuses with lysosomes to form a phagolysosome. 5. Destruction and digestion: O2 increases and ROS is produced. pH conditions continue to lower and antimicrobial peptides damage the foreign invader. 6. Exocytosis: Phagolysosome fuses with phagocytes cytoplasmic membrane. Undigested material is expelled.

First line defenses: 3

Physical barriers block entry of a pathogen, but if invaders breach the barrier, signals are sent out by the immune system. - Skin (outside) Dermis: inner layer of connective tissue Epidermis: out layer if dead epithelial keratin cells Mucous membrane: Line digestive and respiratory tracts and are bathed in mucous secretions (goblet cells secrete mucous) - contain mucociliary mucous/cilia cells (movement out of the respiratory tract) Antimicrobial substances: degrade and destroy foreign microbes - Lysozyme (Found in tears and other bodily secretions, breaks down peptidoglycan layers) - Peroxidases (break down superoxides) - Lactoferrin (removes iron from microbes) - AMP's (antimicrobial peptides ex: defensins that punch holes) Normal microbiota: - Found on skin, mouth, gastrointestinal tract, immune system, urogenital tract - Competitive exclusion: Defends against pathogen and excludes them - Produce toxic compounds: Bacteriocins go after pathogens - Development of immune system: Immune system can tolerate and differentiate them from pathogens Other processes of first-line defenses: Stomach acids, peeing, coughing, saliva, tears, vomiting

Compare and contrast the primary and secondary responses in humoral immunity.

Primary: - 10-14 days for antibodies to accumulate - Naive B cells that bind the antigen present the pep-tide fragments to T H cells. Once those B cells get the second signal from T H cells, they multiply, generating a population of cells that recognize the antigen. As some of the activated B cells continue dividing, others differentiate to form antibody-secreting plasma cells - B cells increase in number Secondary: The secondary response is much faster and more effective than the primary response. - Long lasting immunity - Involves memory B cells

Cytokines

Proteins that function as chemical messengers, allowing cells to communicate.

Primary lymphoid organs

Stem cells: Where blood cells originate. Where B and T first come from. Bone marrow: Where B cells remain and mature. Thymus: Immature cells migrate to the thymus. (Cells cannot come into contact with antigen in these places. Once matured, cells gather and migrate to secondary lymphoid organs to come into contact with antige to initiate immune responses)

Describe the inflammatory process, focusing on the factors that initiate the response and the outcomes of inflammation. Initiation? Outcomes? Purpose of inflammation?

Steps: 1. Foreign invader is first introduced. Tissue blood flow remains normal. 2. Resident macrophages degrade bacteria but need additional assistance. Inflamatory mediators are released and cause small blood vessels to dilate. Phagocytes squeeze through endothelial cells and enter the infected tissue. Neutrophils are first to the infection site. 3. Phagocytes destroy invaders and macrophages ingest dead cells. 5. Clotting factors leak into the tissue to prevent further bleeding. Dead Neutrophils become puss. 1. The inflammatory response is initiated when microbes invade or tissues are damaged. 2. 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. 3. Inflammation helps contain an infection by localization, but the response itself can be damaging.

Describe the key steps of the inflammatory response. In your response, give an example of when the inflammatory response would be needed and please define any terms and be specific and complete in your response. How do phagocytes enter tissues during an inflammatory response?

Steps: 1. Foreign invader is first introduced. Tissue blood flow remains normal. 2. Resident macrophages degrade bacteria but need additional assistance. Inflamatory mediators are released and cause small blood vessels to dilate. Phagocytes squeeze through endothelial cells and enter the infected tissue. Neutrophils are first to the infection site. 3. Phagocytes destroy invaders and macrophages ingest dead cells. 5. Clotting factors leak into the tissue to prevent further bleeding. Dead Neutrophils become puss. Example of when an inflammatory response would be needed? - If someone injures some part of their body, foreign invaders enter and the inflammatory response is triggered. How do phagocytes enter tissues during an inflammatory response? Blood vessels dilate due to inflammatory mediators. Phagocytes squeeze through endothelial cells to enter infected tissue.

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."

Effector Functions of T H (CD4) Cells

T H cells activate cells that present peptides they recognize on MHC class II; various cytokines are released, depending on subset of the responding T H cell. Macrophages and B cells present peptides from exogenous proteins in the groove of MHC class II molecules. Subsets of T H cells direct the immune system to an appropriate response for a given antigen. "

Compare and contrast TH and TC cells with respect to antigen recognition and the response to antigen.

Tc cell receptor: - Does not interact with free antigen, antigen must be presented - TC cells recognize antigens presented on MHC class I molecules. - All nucleated cells present endogenous antigens on MHC class I molecules. - CD marker is CD8 Th cells: - Does not interact with free antigen, antigen must be presented - TH cells recognize antigens presented on MHC class II molecules. - B cells and macrophages present exogenous antigens on MHC class II molecules - CD marker is CD4

Describe the importance of T-cell receptors and CD markers in the T cell response.

Tc cell receptor: - Does not interact with free antigen, antigen must be presented - TC cells recognize antigens presented on MHC class I molecules. - All nucleated cells present endogenous antigens on MHC class I molecules. - CD marker is CD8 Th cells: - Does not interact with free antigen, antigen must be presented - TH cells recognize antigens presented on MHC class II molecules. - B cells and macrophages present exogenous antigens on MHC class II molecules - CD marker is CD4

What are the two types of T cells? Compare and contrast in terms of the following: activation (consider cells, molecules, and circumstances involved), effector function, CD marker, type of antigen each T cell responds to, cells that are impacted by each T cell activation.

Tc/killer cells: Killer cells Target cells impacted: All nucleated cells Function: Induces apoptosis CD marker: CD8 Type of antigen: MHC class 1 presented; Endogenous Cells impacted: Nucleated cells that are cancerous or virally infected Effector function: induced target cell to undergo. apoptosis (programmed cell death) Th cells: Activator cells Target cells impacted: B cells (make antibody) and macrophages function: Activates specific target cells CD marker: CD4 type of antigen: Exogenous; MHC class 2 antigen presentation cells impacted: Tc cells that respond to cytokines produced Effector function: Activates target cell

Compare and contrast the functions of Tc cells and natural killer (NK) cells in the immune response. In your response describe which immune response (innate and/or adaptive) each cell type is a part of, how each becomes activated (if relevant), and the target(s) of each. Why are both cell types considered cytotoxic (define this term)? Be specific and complete in your response.

Tc: - Acquired immunity Activation: Dendritic cells enter secondary lymphatic organs present antigens ti naive at cells. Target: Nucleated cells Nk: - Innate immunity Activation: No activation process. Derived from bone marrow. Target: Virally infected cells without MHC class 1 Both: - Induce apoptosis in infected self cells (programmed cell death) - Look for our own cells that arent behaving the way theyre supposed to. They do so through by releasing a death packahe (granzymes, perfirins, destroy the cell) Different: TC: Adaptive immune response - Show more specifity - Need MHC class I to present to them - Presentation is done by dendritic cells that have the co stimulatory molecule (part of the activation step) TH: Release cytokines to help recuit them. - Go after endogenous antigen. Brings it outside and its present. (Cytotoxic kills the cell) NK: - Innate - Not as specific, use the Fc porion of the antibody - Doesnt need a presentation of MHC classes - Destroys - Binds to an antibody FC portion - Deliver a death package, do not need MHC presentation - Cytotoxic (kills the cell)

1. Describe the steps of complement system activation by the classical pathway, including how it is triggered, each component of complement (proteins by name), and their role in the three major protective outcomes of complement activation (briefly describing each outcome). 2. In your response, explain what the complement system is and its role in the innate immune response. How could a microbe evade the complement system (Discussed in Ch. 16--give at least one example of how evasion may occur)? Be specific and complete in your response.

The complement system involves a series of inactive proteins that flow throughout the system. It is triggered upon an AG-AB complex binding onto the first complement protein. Its main role is to protect the body against any foreign invaders by triggering opsonization, the inflammatory response or cell lysis. Some microbes have C5A peptidase, it destroys C5A and no chemoattractants can be released. This means that phagocytosis cannot occur. Another way a microbe can evade the complement system would be if they contained an M protein that prevents opsonization by binding to c3b which inactivates it. The process of the complement system includes: C1 becomes activated after the complex binds and then activates the next 2 proteins which are C2 and C4. C2 and C4 split into C2A, C2B, C4A, and C4B. C2A and C4B bind together and form an enzyme called C3 convertase (its main function is to split C3). C3 is then split into C3A (inflammation) and C3B (opsonization and cytolysis). C3B combines with C3 in order to make a protein to split C5. C5B combines with compliment proteins C6, C7, C8, and they create a receptor that attracts C9. These complement proteins work together to perform cytolysis and punch holes in the cell membrane. Meanwhile, C5A and C3A work together to create histamines that aid the inflammatory process. 3 Major outcomes: Opsonization: C3B binds to microbial/foreign cells to function as an opsonin. Coating enhances phagocytosis because material that has been opsonized makes it easier for phagocytes to engulf. Inflammation: Inflammatory: C5A chemoattractant draws phagocytes to the area where the complement system has been activated. C3A and C5A cause inflammation, and cause mast cells to release pro-inflammatory cytokines. Cytolysis: Lysis: C5B, C6, C7, C8 and many C9 molecules form membrane attack complexes. Pores form in the membrane which ultimately causes lyses (cell death).

Effector Functions of the Complement System

The major protective outcomes of complement system activation include opsonization, an inflammatory response, and lysis of foreign cells"

Describe the steps of activation of B cells against a T-dependent antigen, beginning with the first encounter with an antigen. Be sure to include the role of T cells and cytokines in your response. In your response, please explain the function of plasma and memory cells as well as the concept of clonal selection and clonal expansion. Briefly describe how is this response different from T-independent activation of B cells. Be specific and complete in your response.

The role of T cells is very different from that of B cells. T cells never produce antibodies. Instead, effector T cells directly interact with target cells to cause distinct changes in those cells. B cells: Activated B cell is an antibody-producing plasma cell. Functional B cell that produced antibody. Antibody: Initiate complement system, recruit NK cells in ADCC, recruit phagocytes. B cells activations by T cells, diffferentiate into plasma cells, What is the antigen? Protein based is T dependent. Protein gives a strong response - Activate cell by a t. helper delivering cytokines. Triggers a strong response - Proliferation, formation of memory cells, longer immunity Plasma cells made. T independent: - Carbohydrate, weak response - No t helper cell is binding, no MHC is involved - B cell is activated due to repeating units. Lypopolysaccharide. Its activated by crosslinking No memory cells, mainly igM produced, no swithcing to iGg T independent: This process is different when compared to T dependent B cell activation. In T independent activation, the cell doesn't rely on the Th cell in order to become activated. The MHC receptor isn't involved either. Instead, the B cell is activated by crosslinking with repeating units such as lipopolysaccharides. No memory cells are produced. Primary response: Slow, but you get rid of it

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 " - First line defense

" The Process of Phagocytosis

The steps of phagocytosis include chemotaxis, recognition and attach ment, engulfment, phagosome maturation, and phagolysosome formation, destruction and digestion, and exocytosis."

B cell receptor

antibody that binds to antigen

Briefly compare and contrast the five classes of immunoglobulins (Ig) (specific classes of antibodies) by function and abundance.

igG: 80-85% (21 days) - Most abundant class in the blood and tissue fluids. • Provides longest-term protection because of its long half-life. • Provides direct protection by neutralizing viruses and toxins, immobilizing motile organisms, preventing microbes from adhering to cell surfaces, and cross-linking antigens. • Binding of IgG to antigen facilitates phagocytosis, leads to activation of the complement 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. IgA: 10-13% (6 days) • 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 IgD: "<1% (3 days) nothing IgE: <0.01% (2 days) • Binds via the Fc region to mast cells and basophils. This bound IgE allows those cells to detect parasites and other antigens and respond by releasing their granule contents. • Involved in many allergic reactions. IgM: 5-13% (10 days) • First antibody class produced during the primary response. • Principal class produced in response to T-independent antigens. • Provides direct protection by neutralizing viruses and toxins, immobilizing motile organisms, 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).

Macrophages

in tissues - abundant in liver, spleen, lymph nodes, lungs, peritoneal cavity - Makes sure the areas stay sterile and free of microbex

Helpter T cell activation and action

look @ slide

Steps of B cell activation by T dependent antigens: requires T helper cells

1. B cell X binds to specific epitope of Ag X. Receptors recognize specific epitope of Ag X = clonal selection. 2. B cell engulfs antigen X. Once engulfed in endosome, it chops up antigen into peptide fragments. 4. On the interior b cells have mhc class 2 molecule. Starts off inside the cell, but once it binds to the fragment, it comes off to the surface to present the M (antigen presentation). Presented to T helpers. 5. They are presented to T helper cells by the B cell. T cell decides if it's harmful or not. 6. If Ag harmful: T helper makes contact with mhc molecule containing fragment and releases cytokines back to the B cell (signaling molecule) which signals for the B cell to activate and differentiation. Activation leads to colonial proliferation: Clones are made of B cell X. Differentiation: -Plasma cells make an antibody specific to Ag X. -Memory cells made for subsequent encounter with AgX, quickly poliferate and differentiate for fast response (secondary response) 7. Harmless: - No cytokines releases - Does not recognize it as a threat and doesnt communicate with the B cell. - The B cell is not activated and becomes anergic (unresponsive to future exposure of Ag).

Understand the overview of the adaptive immune response as described in the summary figure (Figure 15.24)

1. Dendritic cells that have gathered antigen in the periphery present to T cells in the secondary lymphatic organs - B cells are also presented antigen inside of the lymphatic organs, but not by dendritic cells. 2. Naive T and B cell activates, proliferates, differentiates to form effector and memory cells. 3. TC cells induce apoptosis in infected "self" cells; also produce cytokines that alert neighboring cells. 4. TH cells activate B cells that present specific antigen 5. TH cells activate macrophages that present antigen via MHC class II molecules; also produce cytokines that determine other responses. " FIGURE 15.24"

CH 14 SHORT ANSWER

1. Describe how the skin protects against infection. 2. What factors in saliva aid in protection against microbes? 3. Why is iron availability important in body defenses? 4. Name two categories of cytokines and give their effects. 5. What is the function of a TLR? 6. Contrast the pathways of complement activation. 7. How do complement proteins cause foreign cell lysis? 8. How do phagocytes enter tissues during an inflammatory response? 9. How is acute inflammation different from chronic inflammation? 10. Describe the function of apoptosis.

Plama cells

secrete antibody molecules that bind to antigen X

CH14 MULTIPLE CHOICE

1. Lysozyme does which of the following? a) Disrupts cell membranes b) Hydrolyzes peptidoglycan c) Waterproofs skin d) Propels gastrointestinal contents e) Propels the cilia of the respiratory tract 2. The hematopoietic stem cells in the bone marrow can develop into which of the following cell types? 1. Red blood cell 2. T cell 3. B cell 4. Monocyte 5. Macrophage a) 2, 3 b) 2, 4 c) 2, 3, 4, 5 d) 1, 4, 5 e) 1, 2, 3, 4, 5 3. All of the following refer to the same type of cell except a) macrophage. b) neutrophil. c) poly. d) PMN. 4. Pattern recognition receptors (PRRs) detect all of the following compounds except a) peptidoglycan. b) glycolysis enzymes. c) lipopolysaccharide. d) flagellin. e) certain nucleotide sequences. 5. The direct/immediate action of interferon on a cell is to a) interfere with the replication of the virus. b) prevent the virus from entering the cell. c) stimulate synthesis of inactive "suicide enzymes." d) stimulate the immune response. e) stop the cell from dividing. 6. A pathogen that can avoid the complement component C3b would directly protect itself from a) opsonization. b) triggering inflammation. c) lysis. d) inducing interferon. e) antibodies. 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. 8. All of the following cell types are found in a granuloma except a) neutrophils. b) macrophages. c) giant cells. d) T cells. 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. 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.

Where are the receptors found (only focus on PRRS)

1. Sentinel cells: - Macrophages - Dendritic cells 2. Virally infected cells 3 locations: 1. cell surface: detect cell surroundings 2. cytoplasm: detect cell damage 3. phagosomes and lysososomes: detect for ingested components

What are the six protective outcomes of antibodies binding to antigen? Briefly describe each outcome and how each aid in the immune response. Be specific and complete in your response

6 protective outcomes: 1. Opsonization: Phagocytes have receptors for Fc region IgG molecules and are able to engulf antibody coated antigens. 2. Compliment system activation: Antigen-antibody complexes can trigger the classical pathway of compliment system activation. Specific compliment system proteins attach onto the fc portion of the antibody. This leads to a set of reactions. 3. Immobilization and prevention of adherence: Antibodies bind to flagella and pili. This affects attachment and mobilization. Prevents infection. 4. Cross-linking: Antibody dependent cellular toxicity: Antibody links to separate but identical antigen molecules. Creates a big antigen antibody complex. 5. Neutralization: A pathogen coated with antibodies cannot bind to molecules on a cells surface. 6. Antibody-dependent cellular cytotoxicity (ADCC): IgG molecules bind to tumor or virally infected cell. NK cells attach to fc region of IgG and kills target cell.

Describe six protective outcomes of antibodies (antibody-antigen binding).

6 protective outcomes: 1. Opsonization: Phagocytes have receptors for Fc region IgG molecules and are able to engulf antibody-coated antigens. 2. Compliment system activation: Antigen-antibody complexes can trigger the classical pathway of complement system activation. Specific compliment system proteins attach onto the fc portion of the antibody. This leads to a set of reactions. 3. Immobilization and prevention of adherence: Antibodies bind to flagella and pili. This affects attachment and mobilization. Prevents infection. 4. Cross-linking: Antibody links to separate but identical antigen molecules. Creates a big antigen-antibody complex. 5. Neutralization: A pathogen coated with antibodies cannot bind to molecules on a cells surface. 6. Antibody-dependent cellular cytotoxicity (ADCC): IgG molecules bind to tumor or virally infected cell. NK cells attach to fc region of IgG and kills target cell.

protective outcomes of AB-AG binding

6 protective outcomes: 1. Opsonization: Phagocytes have receptors for Fc region IgG molecules and are able to engulf antibody coated antigens. 2. Complement system classical pathway activation: Antigen-antibody complexes can trigger the classical pathway of the complement system. The first complement protein (C1) is activated by attaching onto the AG-AB complex. This leads to a series of reactions. 3. Immobilization and prevention of adherence: Antibodies bind to flagella and pili. This affects attachment and mobilization which ultimately prevents infection. 4. Cross-linking: Antibody links to separate but identical antigen molecules. Creates a big antigen antibody complex. 5. Neutralization: A pathogen coated with antibodies cannot bind to molecules on a cells surface. 6. Antibody-dependent cellular cytotoxicity (ADCC): IgG molecules bind to tumor or virally infected cell. NK cells attach to fc region of IgG and kills target cell.

Describe the role of TH cells in B-cell activation (including clonal selection and expansion).

Activated B cells: These cells can proliferate because their B-cell receptors are bound to antigen and the cells have received required signals from TH cells Activation process: - Naive b cells are gathered in the secondary lymphoid organs where they encounter antigens - B cell's antigen receptor binds to T-dependent antigen. B cell takes in antigen by endocytosis. - Degraded into peptide fragments - Peptide fragment is delivered to MHC class II, moved to surface, and presented. - Th cells inspect, bind to peptide fragment, and activates the B cell. - Colonial expansion is triggered via cytokines. Note: If no T H cells recognize the peptides presented by a B cell, that B cell may become anergic (unresponsive to future exposure to the antigen). This results in tolerance to that antigen.

CH14 Part 1

BEFORE CLASS INNATE IMMUNE RESPONSE

Roles in the classical compliment pathway

C3B: Opsonization. binds to microbe resulting in posonization. Coats it, and enhances phagocytosis. 2. Also works to split c5. C5B will embed itself in a microbe membrane, recruit other C'S. Cytolysis happens due to C's puncturing a hole in the mircobe membrane of a bacterial cell. C5, C6, C7, C8, will form a membrane attack complex. C3A AND C5 A: Inflammation. bind to the surface of mast cells, in the tissue. Causing histamine. C5A also attracts phagocytesE

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."

Describe the classical pathway and how it leads to complement system activation.

Classical pathway: - Antibodies binding to an antigen (invader) to form C3 convertase. (Triggered by antibodies binding to microbial invaders) 1. An antibody binds specifically to a surface molecule (Microbial antigen invader) 2. Antigen antibody complex binds to first compliment protein C1 and becomes activated. It then splits the next 2 molecules. 3. C2 and C4 are split and activated by C1. C2 becomes C2A and C2B, C4 becomes C4B and C4A. 4. C2A binds to C4B and becomes C3 convertase to split C3 into C3A and C3B

Outline the process of clonal selection and expansion. Understand that these events can occur in both B and T cells (though the text describes the details of B cells in 15.10, note that T cells go through a similar process)

Clonal expansion: Each B cell is programmed to make only a single specificity of antibody. When antigen is introduced, only the B cells capable of making the appropriate antibody can bind to the antigen, and only those cells begin multiplying. This generates a population of clones—copies of the specific B cells capable of making the appropriate antibodies. - Applies to both B and T cells Each lymphocyte residing in the secondary lymphoid organs is waiting for the "antigen of its dreams"—an anti-gen that has an epitope to which that particular lymphocyte is programmed to respond. When an antigen enters a lymphoid organ, only those rare lymphocytes that recognize it can respond; the specificity of the antigen receptor they carry on their surface (B-cell receptor or T-cell receptor) determines this recognition

" Cytokines

Cytokines include chemokines, colony-stimulating factors (CSFs), interferons (IFNs), interleukins (ILs), and tumor necrosis factor (TNF). - Cell communications

Soluable ligands

Cytokines: Released by cells and bind to cytokine receptor on the cells, then cell reacts Soluable ligand binds to cytokine surface receptors

General Characteristics of T Cells

Cytotoxic T cells (CD8) recognize antigen presented on major histocompatibility complex (MHC) class I molecules. Helper T cells (CD4) recognize antigen presented on major histocompatibility complex (MHC) class II molecules."

Dendritic Cells

Dendritic cells develop from monocytes; some have other origins. - Cells of the immune system

Activation of T Cells

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"

T H Cell

Effector form of a helper T cell; it activates B cells and macrophages, and releases cytokines that stimulate other parts of the immune system.

Effector T cells

Effector: What job its gonna do MHC class I presents to TC (Killer) Cells - presents endogenous Ag - All nucleated cells present endogenous antigens on Mch class I - If infected it uses the receptor to allow the TC cell to kill the infected cell - endo (made from the body) - binds to one of our cells to kill it - releases preforin to punch holes and granzyme - leads to apoptosis programmed cell death - All cells w/ nucelus that have been virally infected - CD8 cell MHC class II presents exogenous Ag to T helper cells - (outside of the body, not made from us) - T helper binds to mhc class 2 molecule presenting an antigen - Cytokines secrete - proliferation and differentation of T and b cells - peptide antigens recognized - B cell, macrophages - CD 4 cell

Innate Immunity

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

Compare and contrast the general characteristics of humoral immunity and cell-mediated immunity.

Humoral: Involves B cells and antibody response - Humoral immunity ( humor means "fluids") eliminates microbial invaders as well as their toxins from the bloodstream and tissue fluids. B cells are found within the bone marrow. Cell mediated humanity: Involves T cell response - Cell-mediated immunity (CMI) or cellular immunity , deals with invaders residing within a host cell. These invaders are considered intracellular antigens and include viruses and bacteria / cancerous cells replicating within a host cell.

CH14 Part 2

IN CLASS INNATE IMMUNE RESPONSE

Describe the role of dendritic cells in T-cell activation.

- Activate T cells - Immature dendric cells reside in peripheral tissues to take up material that might contain foreign proteins - If the TLR receptor recognizes a pathogen, they take up more material, enter lymphatic vessels and transport them to the secondary lymphoid organs. - They encounter naive T cells, mature, and present antigen to them. - If the T cell recognizes the antigen, it becomes activated.

Colonial expansion: Once a naive B cell becomes activated by Th

- B cell X goes through proliferation. Many versions of B cell X - Some differentiation cells become effector plasma or memory B cells - Plasma cells oval shaped (Release antibody X which is specific for antigen X) - Memory B cells recognize antigen X when its encountered again

Dendritic cells

- Collect antigens and bring to lymphocyes (T and B) Cells. - Adaptive immunity - Activate them

Describe the induction and outcomes of fever.

- Fever is an important host defense mechanism and a strong indication of infectious disease, particularly a bacterial one. 1. Macrophages release pro-inflammatories due to bacterial products being detected in the body. 2. Temperature rises 3. Cytokines travel from the blood to the brain and temp regulating center raises the temperature. 4. The rise in tempera-ture prevents microbes with lower optimum temperatures from growing, giving the immune system time to eliminate the bacteria before they cause too much harm.

Characteristics of adaptive immune response

- Improves as a result of exposure to an antigen - Has specificity (recognizes antigen) - Has memory (stronger and faster response to re-exposure) - First response: Primary - Second response: Stronger since the immune system remembers and learns (Basis for vaccines) - Has tolerance (ability to ignore any given molecule) Can distinguish our own cells vs non self cells

Activated macrophage in comparison to a ordinary macrophage

- Increased in power - Bigger in size, metabolism, larger number of lysosomes, production of toxic compounds, formation of giant cells

Second line: Fever

- Indicator of infectious disease - Temp regulation center in the brain raises during infection in response to pyrogens (fever heat generating substances) pyrogens: endogenous - produced by our body (pyrogenic cytokines) exogenous - produced by the microbe (LPS) Moderate temp: - inflammatory response - phagocytic killing - multiplication of lymphocytes - release of chemoattractants - production of interferons and antibodies - release of leukocytes from the bone marrow

Describe protective roles of natural killer (NK) cells.

- Innate lymphoid cells - Do not have receptors - Induce apoptosis in antibody bound self cells that cannot present antigen - NK cells can do this because they have Fc receptors for IgG molecules on their surface. ( NK cells recognize and destroy stressed host cells that do not have MHC class I molecules) - Attaches to surface of antibodies and delivers preforin and protease granules; initiates apoptosis.

NK cells: Innate lymphoid cells

- Involved in antibody dependent cellular cytoxicity (Virus infects cell, virus prevents host cell from presenting MHC class 1 molecule and cannot target tC cells, Death package is delivered and Nk cell initiates apoptosis in the self cell that lacks MHC, Infected cell undergoes apoptosis) - Go after virally or cancerous infected cells - Does not need to bind to an MHC class 1 molecule - Initiate apoptosis

Humoral response: B lymphocytes

- Involves B cells ( B lymphocytes) - Primary in the humoral response - Develop in the bone marrow - Start with naive B cells -->active B cells, then proliferate/differentiated into plasma cells (make Ab that binds to an antigen = effector cells) Or memory B cells for future encounter

Cell mediated response: T lymphocytes

- Involves T cells - Naive cytotoxic T cells and Naive helper T cells (Become activated with help of dendritic cells and proliferate/differentiate into TH cells and TC cells (both are effector cells) Or they become memory cells

MHC: Major histocompatibility complex

- MHC Class I Molecule - MHC Class II Molecule (They present to different T cells) T helpers: MHC class two presents them Killer cells: Presented by MHC class 1

Examples of chemoattractants

- Microorganism products, phospholipids, chemokines, C5A

Describe the general significance of pattern recognition receptors (PRRs) in the immune response

- Pattern recognition receptors (PRRs) are sensors that allow the body's cells to "see" signs of microbial invasion - If a cell detects microbial invasion, it produces cytokines to alert other components of the defense system. - Many PRRs detect components of certain groups of microbes

T helper cells function

- Release cytokines for recruition or activations (neutrophils, macrophages, NK, B cells) Steps to activation: - Macrophage engulfs, macrophage degrades proteins into peptide fragments, peptide fragments presented, activation of macrophage

T cell activation: look @ chart

- Requires antigen (Ag) presentation by dendritic cells - Dendritics are part of the innate immune response (dendritic cells in the lymphoid organs) - If harmful: 1. Dendritic cells that present also produce co stimulatory molecule 2. Co stimulatory molecule Activates T cells poliferate and differentiatete - If harmless: - Does not produce the co stimulatory molecule cannot respond and undergo apopsitosis. RT cells prevent certain immue responses

B cell activation:

- Requires help of T Helpers - Moves onto colonial expansion

Innate

- born with it - routine protection - looks for pathogens and suspicious activity - non specific response (not targeting a specific pathogen, targets things that don't belong) - pattern recognition - first and second line defenses

FC region

- certain cells (natural killer cells, phagocytes) have FC receptors that recognize and bind to the antibody

Secondline phagocytosis steps

- chemotaxis - recognition and attachment - engulfment - phagosome maturation and phagolysosome formation - destruction and digestion

adaptive

- develops throughout your life - specific response

Phagocytes: Macrophages

- differentiated from monocytes - regenerate lysosomes to maintain killing power - Use lysosomes to kill/degrade invaders

Phagocytes: neutrophils

- early stage inflammation - easily move into tissue

Tc cells

- induce apoptosis in virus infected or cancer self cells - All nucelated cells have MHC class 1 molecule - Cytotoxic t cell will not recognize a cell thats not been infected - if a cell has been virally infected, the cell will present a viral peptide to the Tc cell. It will make contact, recognize and deliver the death package (Perforin, granzymes poke holes and destroy internal cell components)

B cell activation by t independent antigens

- no th cells involved - b cell receptor - crosslinking to repearing subunits - mainly igm - no memory cells

T reg

- prevent action to self antigens - develop tolerance, prevent autoimmunity and other functions

Complement system

- series of proteins in the blood and the fluid that bathes in the tissue - compliment antibody functions - only focus on the classical pathway (triggered by antibodies binding to microbial invaders)

Phagocytosis: the most important part

-Engulfs, digest material including invading microbes - Macrophages are phagocytic cells (differentiated from monocytes, lysosomes maintain killing power, sentinels) Neutrophils are (WBC, important in early stage inflammation, easily move into tissue

Effector Lymphocyte

Differentiated descendant of an activated lymphocyte; it has properties that allow it to help eliminate antigen.

Classical pathway

1. Antibody binds specifically to surface molecule (Antigen) 2. Antigen-antibody complex binds to first complement protein (C1) and becomes activated and splits the next 2 molecules 3. C2 and C4 are split and activated by C1. C2 --> 2A AND C2 B, C4 --> C4B, C4A, 4. c2a binds to c4b and becomes C3 convertase to split C3 into c3a and c3b

Describe phagocytois

1. At site of infection., chemoattractant is released. Recruit ohagocytes to chemotax to that infection site. 2. Recognition and attachment. - Direct recognition: phagocyte binds to surface of microbe like mannose Indirect binding: involves c3b - Receptors bind to c3b or mannose, and projections of membrane come out of phagocyte and enclose it. 3. Create a phagosome vessicle which encolses it. It matures and increases in O2 to create ROS. Fuse with lysosomes to create a phagolysosome. 4. Phagolysosome destroys and digests 6. Spits it out through exocytosis

Second line: Inflammatory response

1. Bacteria enters through the wound - Resident macrophages will degrade bacteria but need help. They initiate cytokines that trigger the inflammatory response. Now macrophages chemotax to the infection site. 2. Vasodilialation. Increase of blood vessel permeability. 3. Neutrophils squeeze between bound cells on the blood vessel. Diapadesis. - They start phagocytosis 4. Infection is now under control and macrophages ingest dead cells. The neutrophils become puss.

Second line defenses

1. Cells in the immune system that originate from cells a part of the bone marrow. Differentiate into different cells Eosinphil, Basophil, Neutrophil, Monocyte, Macrophage

Leukocytes (WBC) Granulocytes

1. Granulocytes: Membrane enclosed structures with granules - Neutrophils (55-65%) - Basophils (0-1%) - Eosinophils (2-4%)

Development of B cells

1. Group branches off into immature B cells (does not have receptors) 2. Mature stage: Receptors form

Classical complement pathway overview

1. Microbe with antigen on it surface. Antibody recognizes the antigen and binds. C1 binds to the complex and becomes activated 2. C1 will bind and split C2 AND C4. 3. When it splits, C2A binds with C4B and Enzyme C3 convertase forms. 4. C3 split into C3B and C3A by C3 convertase. 5. 2. roles pf C3B: Opsonization, and splitting C5. C5 becomes C5B and C5A. C5B --> C6, C7, C8, AND MANY C9 TO GO THROUGH CYTOLYSIS. 5. C3A and C5A involved in inflamatation

Host cell regulation of complement system

1. Regulatory system inactivates C3B, this is why our cell membranes arent attacked, Microbial cells do not have a regulatory process

CH15 SHORT ANSWER

1. What is a secondary lymphoid organ? 2. Diagram an IgG molecule and label (a) the Fc region and (b) the areas that combine with antigen. 3. What are the protective outcomes of antibodies binding to antigen? 4. Which antibody class is the first produced during a primary response? 5. Which antibody class neutralizes viruses in the intestinal tract? 6. Describe clonal selection and expansion in the immune response. 7. How do T-independent antigens differ from T-dependent antigens? 8. What are antigen-presenting cells (APCs)? 9. Describe the role of dendritic cells in T-cell activation. 10. How does the role of natural killer cells differ from cytotoxic T cells?

Lymphocytes

A group of white blood cells (leukocytes) involved in adaptive immunity; B cells and T cells are examples.

Chemokine

A type of cytokine - signal that allow cells to come to a site of infection. Initiate some kind of action - complimentary system

Adhesion Molecules

Adhesion molecules allow cells to adhere to other cells. - Cell communications

T cell receptor

Ag must be presented to T cell by receptor - T cell contains a CD marker

Agranulocytes: WBC

Agranulocytes - Monocytes differentiate into macrophages and dendritic cells then migrate into tissue (3-8%) - Macrophages - Dendritic cells - Lymphocytes differentiate into Nk, T cells and B ells.

The Nature of Antibodies Structure and Properties of Antibodies

Antibodies have a Y shape with an antigen-binding site at the endof each arm. The tail of the YistheFc region. The antibody mono-mer is composed of two identicalheavy chains and two identicallight chains. The variable region contains the antigen-binding site; the constant region encompasses the entire Fc region as wellas part of the Fab regions.

Protective Outcomes of Antibody-Antigen Binding

Antibody-antigen binding results in neutralization, opsonization,complement activation, immobilization and prevention of adher-ence, cross-linking, andantibody-dependent cellular cytotoxicity

Describe the components that make up an antibody and explain how and where it binds to a specific antigen. (Please include the following terms: variable region, constant region, antigen, epitope, antigen-binding site, Fab region, Fc region)

Antibody: Y shaped protein that binds to an antigen Antigen: Part of the pathogen thats capable of stimulating an immune response (include proteins, lipids and nucelic acids). Molecule that reacts with an antibody/antigen receptor on a lymphocyte (B or T cell) Epitope: Distinct regions of the antigen that the adaptive immune system recognizes. The antibody recognize this region and will bind here. Fab region: Arms of the antibody. Bind to the antigen. Fc region: Stem of the antibody Variable region: At the end of Fab region; specificity antigen binding site. Constant region: Fc region and Fab regions. Allows for other components of the immune system to recognize specific classes of antibodies. (IgM, IgG, IgA, IgD, IgE)

Define the terms antigen, T-dependent antigen, T-independent antigen, immunogenic, and epitope (antigenic determinant).

Antigen: Part of the pathogen thats capable of stimulating an immune response (include proteins, lipids and nucelic acids). Molecule that reacts with an antibody/antigen receptor on a lymphocyte (B or T cell) Epitope: Distinct regions of the antigen that the adaptive immune system recognizes. The antibody recognize this region and will bind here. T-dependent antigens: meaning that the responding B cell requires a signal from a T H cell as part of the activation process. T-dependent antigens characteristically have a protein component. "T-independentantigens: can activate B cells without T H cell help. They include lipopolysaccharide (LPS) and molecules with identical repeating subunits, such as some carbohydrates. "immunogenic: is used to describe the relative ability of an antigen to elicit an immune response. Small molecules are usually not immunogenic, meaning that they do not elicit a response.

Antigen

Antigen: is an antibody generator - immunogenic: ability of an antigen to create an immune response (protein antigen: strong response lipid/nucleic antigen: weak response) small antigen: no response/weak Epitopes: Distinct regions on antigen (attached onto the antigen) - different antibodies for different epitopes

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

Cell Death and the Inflammatory Response

Apoptosis is a mechanism of eliminating "self" cells without triggering an inflammatory response; pyroptosis triggers an inflammatory response.

Understand the term apoptosis.

Apoptosis: a programmed cell death that does not trigger an inflammatory response. - Dying cells undergo changes such as (change of shape, enzymes cut DNA, cell pieces bud off, cell shrinkage) - Apoptosis destroys "self" cells without initiating inflammation vs pyroptosis which triggers an inflammatory response.

Overview of the Adaptive Immune Response

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 acti-vated lymphocyte can proliferate, giving rise to effector lympho-cytes and memory lymphocytes.z

B-Cell Activation

B cells present peptides from T-dependent antigens to T H cells for inspection. If a T H 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

Dendritic Cell

Cell type responsible for activating naive T cells.

Phagocyte

Cell type that specializes in engulfing and digesting microbes and cell debris

Briefly understand how affinity maturation and class switching are a part of the primary response.

Changes that B cells undergo: Affinity maturation: - natural selection among proliferating B cells - Spontaneous mutation occures in some actively dividing B cells - Changes in the antibody binding site is one example Class switching: - B cells are meant to differentiate into plasma cells and secrete IgM. - Cytokines that are produced by Th cells may switch a B cell's genetic program make them secrete other antibody classes - B cells in the mucosa-associated lymphoid tissues generally switch to IgA production, providing mucosal immunity.

Opsonization

Coating of an object with molecules for which phagocytes have receptors, making it easier for phagocytosis to occur.

Regulation of the Complement System

Complement regulatory proteins prevent host cell surfaces from activating the complement system via the alternative pathway

Membrane Attack Complex (MAC)

Complement system components assembled to form pores in membranes of invading cells.

Plasma Cell

Effector form of a B cell; it functions as an antibody-secreting factory

TC Cell

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

WBC

Eosinphil, Basophil, Neutrophil, Monocyte, Macrophage - Protect against macroscopic invaders in the blood stream by carrying out various responses

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.

Granulocytes

Granulocytes include neutrophils, basophils, and eosinophils - Cells of the immune system

Major Histocompatibility Complex (MHC) Molecules

Host cell surface proteins that present antigen to T cells

Ch. 15 Adaptive Immune Response-Part 2

IN CLASS WORK

"Cell-Mediated Immunity (CMI)

Immunity involving a T-cell response.

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.

Explain briefly how the interferon response prevents viral replication.

Interferons are cytokines that regulate

" Memory Lymphocytes

Long-lived descendants of activated lymphocytes that can quickly respond when a specific antigen is encountered again. "

Antimicrobial Substances

Lysozyme, peroxidase enzymes, lactoferrin, and antimicrobial peptides inhibit or kill microorganisms" - First line defense

Neutrophil

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

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

" Normal Microbiota (Flora)

Members of the normal microbiota competitively exclude pathogens and stimulate the host defenses. - First-line defense

Exam 4 Problem Set

Memory cells: Come into contact with a virus you've encountered before, binds with memory cells with the receptor on them. The memory cells will initiate differentiation into plasma cells. Skip B cell activation, go into making plasma cells much faster in larger quanitieies. No clonal selection needed. - Capsule or M protein inactivates C3B. M protein and capsule will prevent it from happening. - Avoiding recognition and attachment: Pathogen is bound to the Fc portion, and the pathogen can't bind.

Antigen

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

Mononuclear Phagocytes

Monocytes circulate in blood; macrophages are in tissues - Cells of the immune system

The B-Cell Response: Humoral Immunity

Most antigens are T-dependent antigens, meaning the B cells that recognize them require help from T H cells"

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"

Agranulocytes: NKC

Natural killer cells - Innate lymphoid cells - Assist addaptive immune repsonse - Recognize and kill virally infected host cells - T and B cells

Characteristics of Neutrophils

Neutrophils are the first cell type recruited from the bloodstream to the site of damage.

Describe the first-line defenses, including the physical barriers, antimicrobial substances, and normal microbiota.

Physical barriers block entry of a pathogen, but if invaders breach the barrier, signals are sent out by the immune system.- Skin (outside)Dermis: inner layer of connective tissueEpidermis: out layer if dead epithelial keratin cells Antimicrobial substances: degrade and destroy foreign microbes- Lysozyme (Found in tears and other bodily secretions, breaks down peptidoglycan layers)- Peroxidases (break down superoxides)- Lactoferrin (removes iron from microbes)- AMP's (antimicrobial peptides ex: defensins that punch holes Normal microbiota:- Found on skin, mouth, gastrointestinal tract, immune system, urogenital tract- Competitive exclusion: Defends against pathogen and excludes them- Produce toxic compounds: Bacteriocins go after pathogens- Development of immune system: Immune system can tolerate and differentiate them from pathogens

Lymphocyte Development: 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. "

Primary Lymphoid Organs

Primary lymphoid organs are the sites where B cells and T cells mature

Humoral response: primary vs secondary

Primary: IGM: Low antibodt made IGG: somewhat higher Secondary: IGM: Low IGG: Extremely high secondary response after exposed again

Clonal Selection

Process in which a lymphocyte's antigen receptor binds to an antigen, allowing the lymphocyte to multiply.

Apoptosis

Programmed death of "self" cells that does not cause inflammation. "

Adaptive Immunity

Protection provided by immune responses that improve due to exposure to antigens; involves B cells and T cells.

Pattern Recognition Receptors (PRRs)

Proteins on or in cells that recognize specific compounds unique to microbes or tissue damage, allowing the cells to sense the presence of invading microbes or damage.

" 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 of damage in a cell's cytoplasm. Certain NLRs in macro-phages and dendritic cells allow formation of an inflammasome."

Describe the three outcomes of complement activation (opsonization, inflammation, and lysis of foreign cells)

Roles: - Opsonization: C3B binds to microbial/foreign cells functioning as an opsonin. Coating enhances phagocytosis. Material that has been opsonized makes it easier for phagocytes to engulf. Inflammatory: C5A chemoattractant draws phagocytes to the area where the compliment system has been activated. C3A and C5A cause inflammation, and cause mast cells to release pro-inflammatory cytokines. Lysis: C5B, C6, C7, C8 and many C9 molecules form membrane attack complexes. Pores form in the membrane and causes lyses.

Secondary Lymphoid Organs

Secondary lymphoid organs are the sites at which lymphocytes gather to contact antigens.

Complement System

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

" 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 Surroundings

Some toll-like receptors (TLRs) are anchored in the cytoplasmic membranes of sentinel cells such as phagocytes and cells that line blood vessels. These TLRs detect certain microbial surface components. Membrane-anchored C-type lectin receptors (CLRs) detect certain carbohydrates molecules found on the sur-face of some microbial cells.

second line cell commiunication

Surafe receptors: - Protein cytokine binds to signaling molecule called ligand - receptor ligan binding triggers cell response/effect 1. Surface receptor on target cell 2. membrane surface ligand 3. Ligand is a soluable molecule that moves through surface receptor Cytokines: chemokines: Various cells, chemotaxis interferons: Various cells, antiviral; regulates immune responses interleukins:

Surface Receptors

Surface receptors bind ligands, allowing the cell to detect substances. - Cell communications

Effector Functions of TC (CD8) Cells

T C cells induce apoptosis in cells that present peptides they recog-nize 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. "

Compare and contrast T-dependent and T-independent B cell activation.

T-independent antigens can activate B cells without the aid of T H cells. - Polysaccharides; Lippopolysaccharides; substances that contain evenly spaced epitopes

The Response to T-Independent Antigens

T-independent antigens include polysaccharides that have multiple identical evenly spaced epitopes, and LPS"

" Complement System Activation

The complement system detects microbial cells and antibodies bound to antigens, and is activated in response

Immunoglobulin Classes

The five major antibody classes— IgM, IgG, IgA, IgD, and IgE—each have distinct functions.

Damaging Effects of Inflammation

The inflammatory process can be damaging to the host, and in some cases this is life-threatening. "

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. Acute inflammation is marked by the prevalence of neutrophils; chronic inflammation is characterized by macrophage and giant cell accumulation, and granuloma formation. "

Phagocytosis

The process by which a phagocyte engulfs microbial invaders and debris.

PRR: TLRs

Toll like receptor: - anchored in the membranes of sentinel cells - go after M/PAMPS in the cells

Helper T Cell

Type of lymphocyte programmed to activate B cells and macrophages, and assist other parts of the adaptive immune response.

Cytotoxic T Cell

Type of lymphocyte programmed to destroy infected or cancerous "self" cells.

B Cell

Type of lymphocyte programmed to make antibodies.

Macrophage

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

Nature of antibodies

Variable region: Accouts for specififty Constant region: Allows for other components of the immune system to recognize specific classes on antibodies

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.

Clonal Selection and Expansion of Lymphocytes

When an antigen enters a secondary lymphoid organ, only the lymphocytes that specifically recognize that antigen will respond; the antigen receptor that a lymphocyte has on its surface governs this recognition. Lymphocytes may be immature, naive, activated, effector, or memory cells.

Antibody

Y-shaped protein that binds antigen.

constant region

allows for other components of the immune systems to recognize specific classes on antibodies (globulents)

memory B cells

build immunity by memory

Cytokine binding patterns

cytokines Bind using receptors Pattern recognition receptor: Detect MAMPs (microbial pathogenic associated molecules patterns) - peptidoglycan - lps - flagellin subunits - microbial nucleic acids - mannose - viruses

Inflammatory Response

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

"First-line defenses

prevent entry, sensor systems detect invasion, and effector mechanisms destroy and remove the invader "

Clonal selection

process of immunity

Lymphatic Vessels Lymph

which contains antigens that have entered tissues, flows in the lymphatic vessels to the lymph nodes