Chapter 20- Anatomy 2

Define Vaccination and the three kinds of components

Vaccination, also known as immunization, involves exposing an individual to an antigen to elicit a primary immune response and generate memory cells. Live, attenuated (weakened) - varicella (ex: chicken pox). "Killed"- requires booster-most vaccines. Killed virus, has antigens, but require booster for stronger response. Subunit- toxoid or portion of bacteria; tetanus and diphtheria.

active immunity

a. Active immunity-make antibodies

Outline the 4 basic steps of how exogenous antigens are processed and displayed by Class II MHC molecules

a. Cell phagocytizes a pathogen. b. Phagocytic vesicle fuses with a lysosome; pathogen is degraded and its antigens are fragmented. c. lysosome fuses with a vesicle from RER that contains class II MHC molecules, and an antigen fragment binds to MHC molecule. d. MHC-antigen complex is inserted into cell's plasma membrane. Macrophage or dendritic cell would do this.

Outline the 4 basic steps of how endogenous antigens are processed and displayed on Class I MHC molecules

a. Cell synthesizes either a self-antigen or a foreign endogenous antigen. b. Antigen is broken down by enzymes in cytosol. c. Antigenic determinant (processed antigen) is transported into RER; coupled with a class I MHC molecule. d. MHC-antigen complex leaves RER by a vesicle and is inserted into cell's plasma membrane.

State the 3 Steps of Naïve B Cell Maturation

a. Hematopoietic Stem cells from the Lymphoid line divide in the bone marrow. b. B cells mature in the bone marrow where self-reactive B cells are destroyed. c. Mature Naïve B cells leave the bone marrow and travel to lymphoid organs

State the 4 Steps of B cell activation, clonal selection and differentiation

a. Naïve B cell binds its' antigen to its' B cell receptor and becomes activated. b. Sensitized B cell processes the antigen and presents it on its class II MHC molecules. c. The B cell then binds to TH cell to become fully activated. d. B cells differentiate into (1) Plasma B cells, which secrete antibodies; and (2) Memory B Cells, which are long-lived cells that do not secrete antibodies but will respond to antigens upon a second exposure.

describe the 5 effects of activated complement proteins

a. cell lysis by formation of a membrane attack complex (MAC) complement proteins are inserted in cell membrane of pathogen. b. enhanced inflammation- complement proteins bind to basophil and granules release inflammatory mediators (histamine and heparin) c. neutralization of viruses d. enhancing phagocytosis due to opsonization- making a pathogen easier to phagocytize so it can be ingested. e. clearance of immune complexes. From classical pathway- involved antigens to antibodies.

phase 2 of antibody- mediated immunity

antibodies

complement activation

antibodies activate complement proteins, leading to cell lysis. Antibodies are part of classical pathway

neutralization

antibodies bind pathogenic components of toxins and block toxic effects. Done to venoms

agglutination and precipitation

antibodies clump antigens together to enhance phagocytosis.

self antigens

antigens present on your own cells.

T cell receptor

are found on surface of every T cell; receptor must bind to a specific antigen before cell can become activated.

Class II MHC

are found only on surfaces of antigen-presenting cells. Helper T (Th) cells interact with class II MHC molecules. Class II MHC molecules present exogenous antigens, or those cell takes in by phagocytosis.

cytokines

are proteins produced by several immune cells that enhance the immune response. d. Many cytokines induce "flu-like" symptoms; including fever, chills, and body aches.

classical pathway for activation of complement protein

begins when inactive complement proteins bind to antibodies bound to antigen.

alternative pathway for activation of complement protein

begins when inactive complement proteins encounter foreign cells such as bacteria or may happen spontaneously.

isografts

between identical twins, no rejection because same genetic make-up and identical antigens.

IgE

binds parasitic worm antigens and allergens to basophils and mast cells, and stimulates them to release histamine (allergic reactions). Facilitates inflammation.

adaptive immunity is the same as

cell- mediated immunity

complement protein

consists of 20 plasma proteins produced primarily by the liver; play a critical role in both innate and adaptive immunity. Circulate in their inactive forms; must be activated by a complex cascade of events mediated by enzymes.

xenografts

different species transplant, such as pig and human.

primary immune response

first exposure to an antigen, specific B cell is activated, proliferates and differentiates into plasma and memory B cells; plasma cells begin to secrete antibodies. IgM first secreted. Antibody levels rise more slowly and to lower levels in the primary response. IgG is the next to secrete.

IgM

first type secreted when B-cell is activated; it's the type that RBC Ab's anti-A and anti-B, so agglutination can occur; can activate complement proteins. Potent agglutinating and precipitating agent, functions in complement fixation. #1 secreted when acutely ill.

Class I MHC

found on surface of all plasma membrane on all nucleated cells. Present endogenous antigens, or those synthesized inside cell. Cytotoxic T (Tc) cells interact only with class I MHC molecules.

Antografts

from yourself, skin grafts. Wont reject it.

dendritic cells

function as antigen-presenting cells; present to T cells and some B cells and activate them

secondary immune response

future exposure to same antigen activates memory B cells formed during the primary immune response; antibodies secreted now are more effective as they bind more tightly and have a higher affinity for their antigens. The IgG level rises rapidly and to a higher level in the secondary response. IgM is second to be secreted.

basophils

granules contain chemicals that are inflammatory mediators such as histamine and heparin; involved in allergic responses

TH cells

helper T cells have no phagocytic or cytotoxic abilities. TH cells exert their effects through secretion of cytokines that activate and enhance various components of immune response.

summarize the role of Tc cells

i. Activated TC cell binds to its target cell (could be cancer cells, cells infected with a virus or intracellular bacteria, and any foreign organ such as transplant). ii. Protein called perforin is released and perforates the target cell's plasma membrane. iii. TC cell then releases enzymes that enter the target cell's cytosol and catalyze reactions that degrade target cell nucleus, leading to fragmentation of the target cell's DNA and its death. TC cells can also induce the process of apoptosis , or programmed cell death. iv. TC cell detaches from target cell and looks for another one.

T Cell Activation, Clonal Selection, and Differentiation. Summarize the process by which T cells are activated

i. Cells present antigens on MHC molecules which bind to specific T cell receptors on helper T or cytotoxic T cell clone triggering T cell activation known as clonal selection. ii. TH or TC binds a co-stimulator and becomes activated. c. Activated T cell clones proliferate and differentiate into effector (immediate effects) and memory t cells (responsible for cell-mediated immunological memory).

IgA

in glandular secretions like mucous, tears, saliva; functions in agglutination and neutralization. Found in breast milk and saliva.

what does MHC stand for?

major histocompatibility complex

Primary Immunodeficiency Disorders

may impair either innate or adaptive immunity.

type IV delayed typed hypersensitivity

mediated by T cells rather than antibodies. TH cells recognize antigens bound to MHC molecules and activate and macrophages and TC cells. Poison ivy and oak; tuberculin skin test.

type III immune complex- mediated hypersensitivity

mediated by immune complexes or clusters of soluble antigens bound to antibodies.

corticosteroids

mimic cortisol's anti-inflammatory effects; prednisone.

type I: immediate hypersensitivity

most common type known allergies; First exposure to an allergen: the allergen binds a B cell which triggers B cell differentiation into plasma cells that secrete antibodies. Subsequent exposures to identical allergens in a sensitized individual result in a rapid response that occurs within a few minutes. Local reactions, such as those in the nasal cavity, produce the common symptoms of runny nose and itchy eyes. You are not born allergic, have to be exposed.

allografts

most common type of graft, between two non-identical individuals of same species.

neutrophils

most numerous granulocyte; phagocytes that ingest pathogens and kill with chemicals such as hydrogen peroxide, hypochlorous acid, and lysozyme • Bacterial pathogens • Damage plasma membranes of pathogens • Reside in blood and are recruited to damaged tissues by chemical signals

Autoimmune Disorders

occur self-reactive T cells or B cells that secrete antibodies bind to self antigens, called autoantibodies.

type II antibody- mediated hypersensitivity

occurs when foreign antigens bind to self-antigens; transfusion reactions; self-reactive B cells not destroyed leads to autoimmunity.

IgD

participates in antigen recognition and the activation process. Found exclusively on B cells, has a role in B cell sensitization and activation.

eosinophils

phagocytes that can migrate from blood to tissues where they are needed • Parasitic pathogens • Cover parasites and release contents of their granules • Chemicals from granules damage parasite and either destroy it or make it easier for other immune cells to destroy

phagocytes

phagocytic cells include macrophages, neutrophils, and eosinophils; process by which cells ingest particles and other cells is called phagocytosis a. Agranulocytes known as monocytes exit bloodstream and take up residence in various tissues where they develop into macrophages

clone

population of T cells that respond to one specific antigen; millions of clones in immune system, but only a few cells of each clone exist in body at a given time.

interleukins

produced by leukocytes; stimulate production of neutrophils by bone marrow, stimulate NK cells, trigger production of interferons, and activate T cells.

interferons

produced by macrophages, dendritic cells, NK cells, and cells of adaptive immunity in response to infection with intracellular viruses or bacteria; inhibits viral replication inside host cells.

passive immunity

receive antibodies like Rho-Gam

anti-inflammatory medications

reduce inflammation and pain by blocking enzymes needed for production of prostaglandins and leukotrienes. Nonsteroidal anti-inflammatory (NSAIDS) ibuprofen.

tumor necrosis factor

secreted by macrophages in response to certain bacteria and other pathogens; attracts phagocytes to area of infection and increases phagocytes activity and stimulates phagocytes to release additional cytokines.

self tolerance

self-reactive T cells that are destroyed; prevents T cells from attacking self cells.

what are the nonphagocytic cells?

- NK cells - Dendritic cells - basophils

what are the 2 types involved in antigen presentation

1. Class I MHC 2. Class II MHC

List the 2 different classes of T cells involved in Cell-mediated immunity

1. Helper T (TH) cells or CD4 cells 2. Cytotoxic T (TC) cells or CD8 cells

1st stage of phagocyte response

1. Local Macrophages are activated. First responders are activated within minutes of cellular injury; phagocytize pathogens and damaged cells; contain invading pathogens.

Situations of autoimmune disorders

1. Release of self-antigens not previously encountered by T cells: blood brain barrier and multiple sclerosis 2. Foreign antigens mimic self-antigens: cardiac cells in rheumatic fever (Strep) 3. Cells may inappropriately express Class II MHC molecules: activates T cells that destroy self antigens in Type I DM 4. Certain pathogens nonspecifically activate B cells: produce cytokines SLE

Functions of Secreted Antibodies

1. aggulation and precipitation 2. opsonization 3. neutralization 4. complement activation 5. stimulation of inflammation

bacterial infection

1. bacteria damage cells and induce an inflammatory response, as local macrophages ingest the bacteria 2. neutrophils enter the area in large numbers and phagocytize bacteria 3. macrophages and bacteria enter lymphatic tissue and activate B cells and Th cells

cancer

1. cancer cells damage surrounding cells and induce an inflammatory response 2. NK cells migrate to the area and begin to destroy the cancer cells and secrete interferons 3. dendritic cells ingest cellular debris and migrate to lymph nodes, when they activate Th cells 4. activated Th cells secrete cytokines that stimulate Tc cells to kill cancer cells

common cold

1. infected cells trigger an inflammatory response and secrete interferons 2. interferons prevent infection in neighboring cells and activate natural killer (NK) cells, which lyse infected cells 3. viral particles and cytokines from Th cells activate B cells, which macrophages, ingest dead cells and activate Th cells in lymphatic tissue 4. B cell differentiate into plasma cells, which secrete antibodies that bind and neutralize the virus 5. Th cells secrete cytokines that amplify the immune response, and Tc cells destroy virally infected cells

what are the 3 roles of Th cells

1. innate immunity 2. adaptive cell- mediated immunity 3. adaptive antibody- mediated immunity

what are the 4 stages of phagocyte response

1. local macrophages are activated 2. neutrophils migrate by chemotaxis, margination and diapedesis 3. monocytes migrate by chemotaxis 4. bone marrow increases production of leukocytes

what are the different types of cytokines

1. tumor necrosis factor 2. interferons 3. interleukins

antibody structure

2 heavy (H) and 2 light (L) chains, constant regions where complement-binding sites are found and variable regions where antigen-binding sites are located.

2nd stage of phagocyte response

2. Neutrophils migrate by chemotaxis, margination and diapedesis. Neutrophils migrate chemotaxis to damaged tissue and phagocytize bacteria and cellular debris attracted by inflammatory mediators and activated complement proteins allow them to adhere to capillary wall (margination); increased capillary permeability provides space between endothelial cells for neutrophils to squeeze through into damaged tissue (diapedesis).

Secondary Immunodeficiency Disorders and AIDS:

3. AIDS caused by Human Immunodeficiency Virus 1 (HIV-1), which is spread through contact with infected blood, semen, vaginal fluid, or breast milk. HIV-1 preferentially binds and interacts with cells displaying CD4 molecules so therefore Helper T cells are affected. These patients will therefore have difficulty with both... 4. Currently, there are a number of drug therapies for HIV-1 including reverse transcriptase and protease inhibitors and entry blockers.

3rd response of phagocyte response

3. Monocytes migrate by chemotaxis and become macrophages; phagocytize pathogens and cellular debris.

4th stage of phagocyte response

4. Bone marrow increases production of Leukocytes. Due to cytokines produced by activated phagocytes, leading to elevated number of leukocytes in blood called leukocytosis.

IgG

80% of all Ab's targeting viruses, bacteria; can cross placenta (anti-Rh); function in opsonization, neutralization and activates complement. Only one that can cross placenta from mother to fetus.

Antibody-Mediated Immunity

A. Involves B cells and proteins secreted by B cells, called antibodies also called immunoglobulins or gamma globulins. B cells have B cell receptors that bind to specific antigens, and a group of B cells that bind to a specific antigen is known as a clone . The antibodies secreted by a B cell clone bind to the same antigen as the B cell receptor.

pus

Accumulation of dead leukocytes, dead tissue cells, and fluid leads is called pus (a wound filled with pus is purulent).

describe the 2nd stage of the innate inflammatory response

Activated complement proteins trigger the release of inflammatory mediators from cells such as basophils and mast cells, and act ass inflammatory mediators themselves.

artificially acquired; results

Artificially acquired- through injection of antibodies to toxins or venoms. Result: no memory cells formed, no lasting protection.

active: artificially acquired; results

Artificially acquired- through vaccination. Result: memory cell formation and lasting protection.

phase 1 of antibody- mediated immunity

B Cell Activation, Clonal Selection, and Differentiation

state the cause and effect of fever

Body temperature above normal range between 36 and 38 degrees C. innate response to cellular injury; initiated when chemicals called pyrogens are released from damaged cells or certain bacteria. Act on hypothalamus and lower set point so body responds by increasing body temperature by increasing muscle activity such as shivering. When too high, sweating and vasodilation occur. Anti-pyretic's reduce fever.

pyrogens

Chemicals released from damaged cells or bacteria that will stimulate a fever.

NK cells

Cytotoxic; nonspecifically kill cancerous cells and cells infected with viruses; Secrete antimicrobial cytokine that activates macrophages and enhances phagocytosis

macrophage

First cells to respond to a cellular injury, where they ingest other cells and cellular debris • Macrophages kill pathogens with chemicals, including hydrogen peroxide and hypochlorous acid (active component in bleach) • Function as Antigen-presenting cells (APCs) cells that display portions of pathogens (antigens) they ingest on their plasma membranes • Activate T cells with these antigens that secrete substances that increase activity of macrophages; example of a positive feedback loop

list and describe the 4 cardinal signs of inflammation

Heat- increase blood supply due to warm blood. Swelling- increased capillary permeability due to histamine. Erythema due to heparin (blood thinner). Redness- increased blood to area due to vasodilation due to histamine and bradykinin. Relax smooth muscle in arterioles; allows blood to flow to injured tissues, and area becomes congested with blood (hyperemia). Pain- prostaglandins, bradykinins, pressure on nerves due to edema (swelling). Recruitment of other cells: inflammatory mediators recruit leukocytes to damaged tissue (chemotaxis) particularly macrophages and neutrophils while complement proteins are simultaneously being activated.

stimulation of inflammation

IgE binds mast cells and basophils, and triggers release of inflammatory mediators.

opsonization

IgG coats antigens and binds phagocytes, enhancing phagocytosis.

phase 3 of antibody mediated cells

Immunological Memory. Memory B cells allow B cells to respond more efficiently when the antigen is encountered a second time (Figure 20.23 Table 20.1). memory b cells are responsible for antibody-mediated or humoral mediated immunological memory, which allows B cells to respond more efficiently.

Erythrocytes do not produce

MHC proteins because they do not have a nucleus.

active: naturally acquired

through exposure via infection.

naturally acquired

through passage from mother to fetus, in breast milk.

immunocompetent

thymus "screens" T cells and mediates destruction of those clones that cannot recognize antigens.

antigenic determinant

unique portion of antigen to which receptor binds.

describe the 1st stage of the innate inflammatory response

Release of inflammatory mediators by damaged cells and local mast cells including histamine, serotonin, cytokines, bradykinin, prostaglandins and leukotrienes.

what do these T cells primarily respond to?

Respond primarily to cells infected with intracellular pathogens (viruses and intracellular bacteria), cancer cells, and foreign cells such as those from a transplanted organ.

T cell formation and maturation

T cells formed in bone marrow but migrate to thymus to mature into huge variety of distinct T cells.

naive

T cells remain that have not yet encountered their specific antigens.

effects of T cells

TH and TC cells have very different roles, although they do interact and depend on one another to function properly.

adaptive antibody- mediated immunity

TH cells directly bind to B cells and stimulate them to proliferate and differentiate. Secrete various interleukins that stimulate B cell proliferation and increase antibody production.

adaptive cell- mediated immunity

TH cells secrete cytokine interleukin-2; required to activate Tc cells.

innate immunity

TH cells secrete cytokine interleukin-3 stimulates macrophages to become more efficient phagocytes and to produce interleukin-12, which stimulates TH cells to generate more interleukin-3 in a positive feedback loop.