Unit 3 Objectives

Front 1

IB
List 3 characteristics an antigen must have to be immunogenic.

Back 1

a. have high molecular weight,
b. be chemical complexity,
c. foreignness (recognized as nonself by the body).

Front 2

IB
Define epitope.

Back 2

The actual portions or fragments of an antigen that react with receptors on B-lymphocytes and T-lymphocytes, as well as with free antibody molecules. Usually equivalent to 5-15 amino acids or 3-4 sugar residues.

Front 3

IB
* Describe 3 groups of noninfectious materials that may act as an antigen.

Back 3

a. allergens
b. foreign tissues and cells
c. the body's own cells that the body fails to recognize as "normal self"

Front 4

IA
Compare adaptive (acquired) immunity with innate immunity.

Back 4

Inate refers to antigen-nonspecific defense that is activated soon after exposure to antigens; is present at birth.
Adaptive refers to antigen-specific defense that takes several days to be protective. It developes through out a human's life-time.

Front 5

IA
Define antigen, immunogen, and epitope.

Back 5

An antigen is a substance that reacts with antibody molecules and antigen receptors on lymphocytes. An immunogen is an antigen that is recognized by the body as nonself and stimulates an adaptive immune response.

Front 6

IB
* Define antigen and immunogen.

Back 6

An antigen is defined as a substance that reacts with antibody molecules and antigen receptors on lymphocytes. An immunogen is an antigen that is recognized by the body as nonself and stimulates an adaptive immune response.

Front 7

IB
State what antigens are composed of chemically.

Back 7

Antigens are large molecular weight proteins and polysaccharides.

Front 8

IB
Define hapten and give an example.

Back 8

A small molecule that by itself is not immunogenic but can act as an antigen when it binds to a larger protein molecule. Penicillin and poison ivy allergies.

Front 9

IB
Briefly describe how the body recognizes an antigen as foreign.

Back 9

The body recognizes the antigen as foreing when epitopes of that antigen bind to B-lymphocytes and T-lymphocytes by means of epitope-specific receptor molecules having a shape complementary to that of the epitope.

Front 10

IB
Compare B-cell receptors and T-cell receptors.

Back 10

B-cell receptors are antibody molecules made by that cell and anchored to the outer surface of its cytoplasmic membrane by the Fc portion. They are "Y" shaped and are composed of 4 glycoprotein chains; they can bind directly to epitopes on protein and polysaccharide antigens. T-cell receptors are composed of 2 glycoprotein chains. They can only bond to epitopes that have been placed on the body's cells by MHC molecules.

Front 11

IB
* In terms of infectious diseases, describe 2 categories of microbial materials that may act as an antigen.

Back 11

a. microbial structures
b. microbial toxins

Front 12

IC1
Define endogenous antigen and exogenous antigen and state which class of MHC molecule binds each.

Back 12

Endogenous: produced within human cells during intracellular infections (MHC-I).
Exogenous: antigens that enter from outside the body (MHC-II).

Front 13

IC1
State which type of T-lymphocyte recognizes epitopes from endogenous protein antigens on MHC-I molecules and which type recognizes epitopes from exogenous protein antigens on MHC-II molecules.

Back 13

The TCRs and CD8 molecules on T8-cells and CTLs recognize endogenous epitopes bound to MHC-I molecules. CD4 and TCRs on T4-cells recognize exogenous epitopes bound to MHC-II.

Front 14

IC1
State the role of proteasomes in binding of peptides from endogenous antigens by MHC-I molecules.

Back 14

Proteasomes are organells that degrade antigen parts being synthesized in the cell in to epitopes by means of proteases and peptidases.

Front 15

IC1
State the role of lysosomes in binding of peptides from exogenous antigens by MHC-II molecules.

Back 15

After exogeous antigens enter APCs through phagocytosis, the lysosomes fuse with the phagosome and degrade the microbes with proteases into a series of peptides or epitopes.

Front 16

IC2
Name two types of cells that function as antigen-presenting cells.

Back 16

Macrophages and dedritic cells.

Front 17

IC2
State the overall function of APCs in adaptive immunity.

Back 17

The over all function of APCs is to activate T4-lymphocytes that have a TCR that recognizes the antigens they are presenting on the MHC-II molecules.

Front 18

IC3
Describe the overall function of B-lymphocytes and their activation by T-dependent antigens in terms of the following:
a. the antigen receptor on their surface
b. how they "process" exogenous antigens
c. the type of MHC molecule to which they attach peptides
d. the role of lysosomes in binding of peptides from exogenous antigens by MHC-II molecules.
e. the type of cell to which they present peptides
f. the types of cells into which activated B-lymphocytes differentiate

Back 18

In order for B-cells to proliferate or become antibody-secreting plasma cells, they must react with T4-cells. First, B-cells bind to epitopes on antigens and engulf them. The antigens are then broken down by lysosomes into peptides epitopes which attach to cell surface by MHC-II. T4-cells recogize the epitope/MHC-II with CD4 and TCRs. The T4s secrete cytokines which cause B-cells to proliferate and differenciate into antibody secreting plasma cells.

Front 19

IC4
Describe the overall function of T4-lymphocytes and their activation in terms of the following:
a. the role of their TCRs and CD4 molecules
b. what they recognize on APCs
c. co-stimulatory signals for activation
d. the role of APCs in T4-lymphocyte activation

Back 19

TCRs and CD4s recognize specific MHC-II/epitope complexes on APCs. costimultory signals, necessary for activation, also occur at this time between APCs and T4-cells. Activated T4s can then produce cytokines that cause B- and T-lyphocytes to proliferate and differenciate.

Front 20

IC4
State the overall function of T4-lymphocytes in adaptive immunity.

Back 20

To produce cytokines that allow B- and T-lymphocytes to prolifferate and differenciate. They also activate NK cells. This is necessary to produce enough lymphocytes to mount an effective immune responce.

Front 21

IC4
Describe the overall function of T8-lymphocytes and their activation in terms of the following:
a. the role of their TCRs and CD8 molecules
b. co-stimulatory signals for activation
c. the type of cells into which activated T8-lymphocytes differentiate
d. what CTLs recognize on infected cells and tumor cells
(recomend reading text)

Back 21

The binding of CD8 and TCRs to MHC-I/endogenous epitopes with specific corresponding shape on surface of infected or tumor cells activate the T8-cells. They also need cytokines from T4-cells to differenciate into CTLs and some into T8-memory or T8-suppressor cells.

Front 22

IC4
State the overall function of T8-lymphocytes in adaptive immunity.

Back 22

One of the body's major defenses against viruses, intracellular bacteria, and cancers by the destruction of infected cells and tumor cells.

Front 23

IC7
Compare Th1 and Th2 lymphocytes in terms of the following:
a. the cytokines they produce
b. whether they promote cell-mediated immunity or antibody production.

Back 23

Th1 cells promote cell-mediated immunity by producing Il-2, INF-gamma, and TNF-alpha. Th2 cells promote humoral immunity by producing Il-4,5,9,10,13.

Front 24

IC8
Briefly decribe NK cells.

Back 24

These cytolytic lymphocytes are designed to kill mutant or virus-infected cells by either killing cells that have antibodies attached through ADCC or that lack MHC-I molecules.

Front 25

ID
Compare and give examples of the following:
a. primary lymphoid organs
b. secondary lymphoid organs

Back 25

a. T- and B-lymphocytes are produced in them. Thymus and bone marrow.
b. Contain T- and B-lymphocytes and APCs. Using these cells, allow body to detect antigens. Lymph nodes and spleen.

Front 26

ID
Define the following:
a. plasma
b. tissue fluid
c. lymph
d. lymph vessels

Back 26

a. liquid portion of the blood
b. plasma that has entered the tissue
c. fluid from tissue that has enterened lymph vessels
d. vessels that are responsible for flow of lymph.

Front 27

ID
Briefly describe the importance of the lymphoid system in adaptive immune responses.

Back 27

It ensures that antigens will eventually be recognized by the body and iniate adaptive responces

Front 28

IE
List the 5 general steps involved in the immune responses in their correct order.

Back 28

1. The antigen encounters B- and T-lyphmocytes and APCs
2. Naive lymphocytes must recognize epitopes on the antigen by means of receptors and be activated.
3. After binding, the lymphocytes must prolifferate (clonal selection).
4. Clones differenciate into cells capable of directing body defenses
5. Some lymphocytes differenciate into memory cells capable of anamnestic responce.

Front 29

IE
State where antigens may encounter APCs, B-lymphocytes, and T-lymphocytes if they enter the following:

a. the blood
b. tissues
c. the respiratory tract
d. the gastrointestinal tract
e. the genitourinary tract
f. the skin

Back 29

a. the spleen
b. lymph nodes
c. tonsils, BALT, and MALT
d. Peyer's patches and GALT
e. MALT
f. SALT

Front 30

IE
Briefly describe how the receptor molecules on the surface of naive B-lymphocytes, T4-helper lymphocytes, and T8-lymphocytes eventually recognize or bind epitope, indicating the roles of BCR, TCR, CD4, CD8, MHC-I, and MHC-II molecules in lymphocyte activation.

Back 30

B-lymphocyte receptors BCR bind to corrosponding epitopes on antigens. T4-lymphocytes use CD4 to recognize MHC-II on APCs and TCR to recognize the epitope itself. T8-lymphocytes use CD8 to recognize MHC-I on any cell and TCR to bind to epitopes attched to the MHC-I.

Front 31

IE
* State the overall function of T4-helper lymphocytes and the importance behind rapid proliferation of activated lymphocytes.

Back 31

T4-cells allow the prolifferation of lymphocytes. Large numbers of lymphocytes are need to launch an effective immune responce.

Front 32

IE
State what types of effector cells the proliferating B-lymphocytes and T8-lymphocytes differentiate into in order to destroy or neutralize the antigen.

Back 32

Plasma cells and CTLs respectively.

Front 33

IE
Define cytokine.

Back 33

Chemokines that promote inflammation and prolifferation of lymphocytes

Front 34

IE
State the function of memory cells.

Back 34

Initiate a rapid, heightened secondary responce against the antigen that stimulated their production.

Front 35

IE
State what is meant by immunologic tolerance.

Back 35

The body becomes tolerant of its own molecules and they don't stimulate an immune responce.

Front 36

IIA
Define antibody.

Back 36

Specific glycoprotein configurations produced by B-lymphocytes and plasma cells in responce to a particular antigen and capable of reacting with that antigen.

Front 37

IIA
In terms of infectious disease, state what humoral immunity is most effective against.

Back 37

Against bacteria, bacterial toxins, and viruses prior to them entering cells.

Front 38

IIA2
* Describe an antibody molecule.

Back 38

Composed of two heavy glycoprotein chains with varied high molecular weights and two light ones, all of which are connected by disulfide and non-convalent bonds.

Front 39

IIA2
Draw the "stick figure" structure of IgG, indicating the Fab and Fc portions.

Back 39

Fab Fab
Y
FC

Front 40

IIA2
* State the functions of the Fab and the Fc portions of an antibody.

Back 40

Provide specificity for binding epitopes on an antgen. Activate complement pathway, bind to phagocytes, bind to mast cells and basophils, and bind to NK cells.

Front 41

IIA2
State what is meant by the biological activity of an antibody.

Back 41

The ability to bind to receptors on phagocytes, mast cells, or basophils and the ability to activate the complement pathways. Resides in the Fc portion of an antibody molecule.

Front 42

IIA2
Compare the structure of IgM and secretory IgA with that of IgG.

Back 42

IgM is composed of 5 monomers (pentamer) connected by J chain, IgA of 2 (dimer) connected by J chain and stablized to resist enzymatic digestion, and IgG of 1 monomer.

Front 43

IIA3
State the characteristics of the following antibody: IgG

Back 43

Monomer, activates classical pathway, binds to macrophages and neutrophils, binds to NKs, crosses the placenta

Front 44

IIA3
State characteristics of the following antibody: IgM

Back 44

Pentamer, first antibody produced, activates classical pathway, functions as B-cell receptor or sIg,

Front 45

IIA2
State characteristics of the following antibody: IgA

Back 45

Dimer, mainly in bodily secretions, Fc portion of secretory IgA binds to components of mucous.

Front 46

IIA3
State the characteristics of the following antibody: IgD

Back 46

Monomer, functions as B-cell receptor or sIg.

Front 47

IIA3
State the characteristics of the following antibody: IgE

Back 47

Monomer, binds to mast cells and basophils to promote allergic reactions and inflammation,

Front 48

IIA4
Define gene translocation and relate it to each B-lymphocyte being able to produce an antibody with a unique shaped Fab.

Back 48

The movement and joining of genes from different locations along chromosomes to produce a new functional coding unit. The heavy chain of antibodies is coded for by VH, DH, or JH, and the light is coded for by VL and JL; the DNA of B-cells contain numerous forms each of these genes. Random gene splicing will produce any combination of the genes.

Front 49

IIA6
Briefly describe the process of antigen recognition and antibody production in the body by indicating the role of:
a. B-lymphocytes and B-cell receptors (sIg)
b. APCs, MHC-II, Il-1, TNF-alpha
c. T4-helpers, TCRs, CD4, and cytokines like IL-2,4,5,6,10
d. costimulatory factors
e. plasma cells
f. B-plasma cells

Back 49

Antigens must first encounter APCs or lymphocytes able to recognize them. B-lymphcytes use B-cell receptors to recognize the antigen. B-cells and APCs use MHC-II to present the antigen to T4-cells which can recognize it using CD4 and specific TCRs. This activates them, causing the T4s to produce IL-2, allowing prolifferation and differenciation into T-cells that either promote cell imunity (Th1) through cytokines like Il-2, or antibody production (Th2) by recognizing antigens from B-cells and producing Il-4,5,10, ect. Costimulatory factors are necessary for B-cells to activate T4s with cytokine TNF-alpha and Il-1. Activated B-cells differeciate into antibody secreting plasma cells; a few become memory cells capable of an anamnestic responce.

Front 50

IIA6
State where in the body antibody production takes place and where antibodies are found after production.

Back 50

Production takes place in secondary organs and antibodies can be found in plasma and lymph.

Front 51

IIA7
* In terms of humoral immunity, discuss what is meant by anamnestic response.

Back 51

Anamnestic responce is a heightened to produce vast quantites of antibodies quickly becaues of the presence of B-memory cells and T4-memory cells that accelerate the immune responces.

Front 52

IIA7
Briefly describe why there is a heightened secondary response during anamestic response.

Back 52

A pool of fine tuned B-memory cells and T4-memory cells remain in body due to clonal expansion and affinity maturation and are able to react immediately if they encounter the antigen that stimulated their production.

Front 53

1C1
State which body cells display MHC-I surface molecules and which cells normally display MHC-II surface molecules.

Back 53

MHC-I molecules are made by all nucleated cells in the body. MHC-II molecules are primarily by antigen presenting cells (macrophages, dendritic cells, B-lymphocytes).

Front 54

IIB1
List 8 ways that antibodies help to defend the body.

Back 54

1. Opsonization
2. MAC cytolysis
3. Neutralization of Exotoxins
4. Antibody Dependant Cellular Cytotoxisity (ADCC) by NKs
5. Neutralization of viruses
6. Blocking bacterial adherence
7. Agglutination of microbes
8. Immobilization of bacteria and protozoans.

Front 55

IIB2
* Discuss the how antibodies defend the body by way of opsonization.

Back 55

Fab part if IgG or IgM bind to epitopes of an antigen. Fc part of IgG can then bind to phagocytes and both antibodies can activate the classical complement pathway, creating C3b and C4b, both of which can act as opsonins.

Front 56

IIb2
* Briefly describe 5 different ways bacteria may resist opsonization.

Back 56

1. some capsules prevent formation of C3 convertase and thereofre C3b, C4b, and other proteins.
2. Some have an affinity for serum protein H that will degrade C3b.
3. Some capsules cover the C3b that does bind prevent opsonization
4. Some capsules are made of human-like carbos against which antibodies are not made.
5. Some bacteria use secretion system III to degrade actin microfilaments needed for phagocytosis

Front 57

IIB3
State specifically how MAC cytolysis protects against the following:
a. gram-negative bacteria
b. "foreign" human cells
c. enveloped viruses

Back 57

a. penetrates the outer membrane and possibly the cyto as well
b. causes direct cell lysis
c. damages the envelope

Front 58

IIB4
* Discuss the how antibodies defend the body by way of ADCC by NK cells.

Back 58

Nks have receptors on surface for Fc part of antibodies. When antibodies have been made aginst antigens on cells, their Fab portion reacts with the antigen and the Fc portion binds to the NK cell, allowing it kill using perforins and granzimes

Front 59

IIB5
Describe how the ability of bacteria to sense their own population density, communicate with each other by way of secreted factors (cell-to-cell signaling), and behave as a population rather than as individual bacteria most likely plays an important role in pathogenicity for many bacteria.

Back 59

Some bacteria will wait to secrete toxins until the population is large enough to produce quantites sufficient to over power the bodies defenses.

Front 60

IIB6
* Discuss the how antibodies defend the body by way of neutralizing viruses.

Back 60

They prevent viral adsorption by covering the viral surface and thereby stopping viral replication.

Front 61

IIB6
* Briefly describe 2 different ways viruses may resist neutralizing antibodies.

Back 61

1) anagenic drift and shift allows the virus to constantly change its epitopes and the origional antibodies don't work any more.
2) high mutation rate and intracellular recombination allows HIV to evade defenses.

Front 62

IIB9
* Discuss the how antibodies defend the body by immobilizing bacteria and protozoans.

Back 62

Antibodies made agains motility organelles prevent the microbes from spreading.

Front 63

IIC1
Give an example of naturally acquired active immunity.

Back 63

The body responds to an antigen and makes its own antibodies.

Front 64

IIC2
Define and give at least one example of each of the following types of immunity:
a. artificially acquired active immunity
b. artificially acquired passive immunity

Back 64

a. immunization with an antigen. Immunization with antenuated microbes (living but non-virulent)
b. injection of the body with antibody containing serum. Using RIG to prevent rabies.

Front 65

IIC2
State what DTaP stands for and what specifically is being injected with the DTaP vaccine.

Back 65

Diptheria, tetanus, and acellular pertusis. Diptheria and tetanus components are toxiods, pertusis is a vaccine produced by recombinant DNA.

Front 66

IIC2
Briefly compare active immunization with passive immunization in terms of tetanus prophylaxis.

Back 66

Td is used if a person has had fewer than three doses of tetanus vaccine they probably have no memory cells for the antigen. If the wound is clean and minorthey are only given Td, in any other case with fewer than three previous doses, both Td and TIG vaccines are used. Td is active immunization and will last a long time, TIG is passive and will be short lived. (look at text)

Front 67

IIC2
Define adjuvant.

Back 67

A substance that an antigen in vaccine may be adsorbed to in order to increase the persistance of the antigen in the body and highten the immune responce but that is non-toxic.

Front 68

IIC2
In artificially acquired immunity, active immunization is preferred over passive immunization. Explain why.

Back 68

Active immunization is longer lived because it causes the body to create its own antibodies and memory cells. Passive immunity is short lived, since it is simply the injection of serum that contains antibodies and doesn't cause the body to produce its own antbodies or memory cells; it also has higher risk of serum sickness.

Front 69

IIC2
* A patient with a deep puncture wound who has never received a DTP vaccination is given both Td and TIG. Another patient with an identical wound and who had 4 DTP vaccinations as a child and a Td booster 3 years ago is given nothing. Discuss the reasoning behind this.

Back 69

The patient who has had no previous immunizations has no memory cells and is at high risk for infection because of the nature of the wound, so both active and passive immunity is used to stimulate antibody production and provide immediate protection. The patient who has revieced multiple immunizations porbably has memory cells agains tetanus and so is able to mount an effective responce without further immunization.

Front 70

IID
* Define monoclonal antibodies, describe how they are produced, and state 4 potential clinical uses.

Back 70

Antibodies of a specific type coming from a clone of identical B-lymphcytes. The spleen of an animal infected with the antigen is removed and the plasma cell producing the desired antibody is removed, fused with a cancer cell so it can live in synthetic environment, and becomes a hybridoma cell. This cell produces in large numbers the desired antibody. They are useful in medical research, serology, to induce immunosuppression, and against viruses and bacteria.

Front 71

IID
Briefly describe immunotoxins.

Back 71

Antibodies against cancer cells that have been attached to radioactive substances or cytotoxins that are therefore designed to carry the poisons to these cells only.

Front 72

IC6
State how CD4(-)CD8(-) T-lymphocytes are activated.

Back 72

They are activated by lipids and glycolipids presented by CD1 molecules on the surface of APCs

Front 73

IC2
Describe the overall function of antigen-presenting cells (APCs) in terms of the following:
a. how they "process" exogenous antigens
b. the types of MHC molecule to which they attach peptides
c. the role of lysosomes in the binding of peptides from exogenous antigens by MHC-II molecules.
d. the types of cells to which they present peptides
e. the role of toll-like receptors in the production of co-stimulatory molecules

Back 73

APCs engulf exogenous antigens and lysosomes fuse with the phagosomes, breaking down antigen into series of peptides. Vesicles containing MHC-II molecules fuse with peptide containing endosomes and MHC-II binds to the epitopes. The MHC-II/epitope complexes are then transproted to the cytoplasmic membrane where they can bind to the TCRs and CD4s on T4-cells. For T4-cells to bind to MHC-II with epitopes, toll-like receptors on the APCs must have bound to pathogen-associated molecular patterns and released costimulatory molecules.

Front 74

IIA5
* Briefly describe the process of clonal selection and clonal expansion.

Back 74

Selection: the B-lymphcytes comes in contact with and reacts with the epitopes that fit its specific sIg. Expansion: the proliferation of activated B-lymphocytes by means of cytokines produced by T4-helpers.

Front 75

IIB3
* Describe 2 ways gram-negative bacteria may resist cytolysis.

Back 75

Some attach sialic acid to LPS O antigen, preventing formation of C3 convertase, others lengthen the LPS O chain which prevents the formation of MAC

Front 76

IIB8
* Discuss how antibodies defend the body by agglutinating microorganisms.

Back 76

Antibodies like IgA and IgM link microbes together so they are removed from lymph and more easily phagocytosed.

Front 77

Briefly describe the process of antigen recognition in cell-mediated immunity and how cell-mediated immunity defends the body. Indicate the role of:
a. antigen presenting cells (APCs), MHC-II and exogenous antigens, MHC-I, and endogenous antigens
b. T4-helper lymphocytes, TCR, and CD4
c. co-stimulatory molecules
d. T8-lymphocytes, TCR, and CD8
e. cytokines
f. cytotoxic T-lymphocytes (CTLs), TCR, CD8, perforin and granzymes, and apoptosis
g. T-memory cells
h. T8-suppressor cells

Back 77

review text!!!!!!!!!!!!!!!!!!!!!!!

Front 78

IIIA
Briefly compare humoral immunity with cell-mediated immunity.

Back 78

Humoral immiunity involves productionof antibodies and is mediated by B-lymphocytes. Cell mediated imunity involves production of CTLs, activation of macrophages and NKs and production of cytokines and is mediated by T-lymphocytes.

Front 79

IIIA
Define cell-mediated immunity and state what it is most effective against.

Back 79

Immunity that involves the activation of macrophages and NKs, production of CTLs, and release of cytokines. Is most effective against virus infected cells.

Front 80

IIIB
Compare the roles of Th1 and Th2 lymphocytes.

Back 80

Th1: recognize antigens presented by macrophages and heighten cell-mediated immunity with cytokines like Il-2 (differencation and proliferation), TNC-gamma (activates NKs and macrophages). Th2: recognize antigens presented by B-lymphcytes and produce cytokines (IL-4,5,9,10,13) that promote antibody production.

Front 81

IIIC1
* Describe cytotoxic T-lymphocytes and indicate how they can react with and destroy virus-infected cells, cells containing intracellular bacteria, and cancer cells without harming normal cells. Also state the mechanism by which cytotoxic T-lymphocytes kill these cells.

Back 81

CTLs are designed to remove body cells desplaying foreign epitopes. They do this by a) intracellular granzymes. Binding of MHC-I and epitope with corresponding TCR and CD8 causes CTL to release perforin, increasing infected cell's permeability and allows released granzymes to enter, which trigger cell apoptosis. b) triggering apoptosis through FasL/Fas interactions. By either means the cell breaks into enveloped fragments and is removed by macrophages.

Front 82

IIIC1
Briefly describe two ways certain viruses may evade cell-mediated immunity.

Back 82

1. high rate of mutation allows some viruses to change epitopes to unrecognized shapes.
2. Some viruses prevent infected cell from producing MHC-I so one foreign epitopes are placed on surface for CTLs to recognize.

Front 83

IIIC2
*Describe how NK cells are able to recognize and destroy infected cells and cancer cells lacking MHC-I molecules.

Back 83

NKs have killer-activating receptors that bind to a number of normal human molecules, this kill mechanism is only turned off if the killer inhibitory receptor binds to MHC-I. If MHC-I is not present the killer-activating receptors cause NK to insert perforin into aborant cell and inject granzymes.

Front 84

IIIC2
*Briefly describe how Th1 cells may help to destroy intracellular organisms inside of the phagosomes and lysosomes of macrophages and help control HIV while Th2 interfere with this process.

Back 84

Th1 cytokine interferon-gamma prompts macrophges to produce TNF and toxic oxygen that destroy organisms living in phagosomes; the cytokines Il-4 and 10 produced by Th2 cells interfere with interferon-gamma.

Front 85

IIIC3
* Describe how interferon prevents viral replication.

Back 85

Interferon induce uninfected cells to produce enzymes able to break down mRNA which are inactive unless the cell becomes infected and will kill both virus and cell when active

Front 86

IIIC3
Interms of cell-mediated immunity, describe how granuloma form.

Back 86

Cytokines are continuously secreted from area infected with microges that are hard to remove results in acculumlation of densely packed macrophages which release cytokines that cause formation of granuloma and scar tissue.

Front 87

IIID
* Briefly describe what is meant by adoptive immunotherapy.

Back 87

Refers to artificially increasing the number of specific immumocompetent cells or altering tumor cells to make them more immunogenic.

Front 88

IIID
State what is meant by immune modulation and state 4 examples of agents being tried as immune modulators.

Back 88

Attempt to improve body's immune responces artificially through therapeutic use of cytokines, cell receptors or other proteins produced through recombinant DNA technology. (IL-2, INF-alpha, beta, and gamma)

Front 89

VA
Define the following:
a. primary immunodefiency
b. secondary immunodeficiency

Back 89

a. a genetic defect in the immunresponces one is born with.
b. secondary factors causes decrease in immune responces, one is not born with it

Front 90

VB
List 3 different types of primary immunodeficiency indicating how humoral and cell-mediated immunity is affected in each case and how each may be treated.

Back 90

1. B-lymphocyte disorders: decreased humoral immunity but cell-mediated is normal. Treated with artificially aquired passive immunization.
2. T-lymphcyte disorders: little or no cell-mediated immunity, humoral immunity may be affected if T4-helpers are. Treated with thymus transplat.
3. Combined T and B-lymphocyte disorders: little or no cell-mediated or humoral immunity. Patient is kept in sterile isolation, sometimes given bone marrow transplant.

Front 91

VC
State what is meant by secondary immunodeficiency and list 4 possible contributing factors.

Back 91

Some secondary factor inhibits the immune responces can be induced by factors such as malnutrition, viruses, X-rays, aging, cancers, etc.

Front 92

VI
Define the following:
a. immediate hypersensitivity
b. delayed hypersensitivity

Back 92

a. refers to humoral immunity causing harm.
b. refers to cell-mediated immunity causing harm.

Front 93

VIB1
* Describe the mechanism for Type I (IgE-mediated) hypersensitivity, give several examples, and state how they are treated symptomatically.

Back 93

Fc protion of IgE (present in huge numbers in allergic peoples) binds to surface of basophils and mast cells, when allergen crosslinks Fab portions, histamines and other proinflammatory mediators are released. Allergens include hair, pollen, dust, etc and are treated with steriods, antihistamines, epinephrines, and sodium cromolyn.

Front 94

VIB1
Describe how desensitization (allergy) shots work to lessen the severity of Type I hypersensitivities.

Back 94

exposeure to dilute samples of allergen stimulates production of IgG and IgA, which act as blocking antibodies to neutralize the allergen. Shots also appear to supress production of IgE by inducing tolerance and production of T8-suppressor cells.

Front 95

VI
Briefly describe how monoclonal antibodies against the Fc portion of IgE may someday be used to prevent Type I allergies.

Back 95

Monoclonal antibodies are made against the Fc portion of IgE preventing it from binding to basophils and mast cells.

Front 96

VI
* When a person has hay fever, common symptoms include runny eyes, runny nose, swollen sinuses, and difficulty in breathing. In terms of humoral immunity, discuss the mechanism behind these symptoms. Also state the reason for giving antihistamines.

Back 96

The symptoms are induced by the inflammatory agents released when the IgE on basophils and mast cells encounter the allergen during the allergic reaction. Antihistamines block histamine from binding to receptors.

Front 97

VI
Describe the mechanism for Type II (antibody-dependent cytotoxicity) hypersensitivity and give 2 examples.

Back 97

IgG or IgM is made agianst normal self antigens or foreign epitopes that resemble molecules on host cells. This leads to opsonization of host cells, MAC of host cells, ADCC destruction of host. AB and Rh blood group reaction, autoimmune diseases.

Front 98

VI
Describe the mechanism for Type III (immune complex-mediated) hypersensitivity and give 2 examples.

Back 98

Soluble antigen-antibody complexes form in large amounts and lodge in capillaries and membrane surrounding them and activate classical complement pathway causing massive inflammation, influx of neutrophils, MAC lysis, aggregation of platelets. Serum sickness and rheumatoid arthritis.

Front 99

VIC
Describe the mechanism for Type IV (delayed) hypersensitivity and give 2 examples.

Back 99

T8-lymphocytes become sensitized to an antigen while Th1 cells are also sensitized to the same antigen and produce cytokines. Poison ivy and type-1 diabetes.

Front 100

VID
Define superantigens, state why they are able to activate exceedingly large numbers of T4-lymphocytes, and give 3 examples of superantigens.

Back 100

Bacterial toxins that react with excedingly large numbers of T4-lymphocytes. They can do this because they bind directly to outside of MHC-II molecules and so activate many T4s. TSST-1, Spe, SE.

Front 101

IC3
Briefly describe how TI-1 and TI-2 antigens activate B-lymphocytes.

Back 101

TI-1 amtigens(LPS, bacterial DNA etc.) bind directly to toll-like receptors on B-cells to activate them.
TI-2 antigens, such as capsular polysaccharides, activate B-cells by cross-linking a number of B-cell receptors.

Front 102

IIB3
* Discuss the how antibodies defend the body by way of MAC cytolysis.

Back 102

The antibodies IgG and IgM bind to an epitope on a membrane and activate the complement pathway, allowing the MAC (C5b6789n) to put holes in the membrane.

Front 103

IIC
Define the following:

a. active immunity
b. passive immunity

Back 103

a.antigens enter the body and stimulate production of antibodies and B-cells and is longer lived.
b. body recieves antibodies made in another person or animal and is short lived

Front 104

IIC1
Give two examples of naturally acquired passive immunity and state why this is important to newborns and infants.

Back 104

Placenta trasfer of IgG; IgA and IgG in human colostrum and milk that nursing babies drink. These are necessary to protect the babies from infection while they are still developing their own immune system.

Front 105

IV
.** In terms of humoral immunity and cell-mediated immunity, describe how the body defends itself against viruses by:
a. destroying the virus (2 ways)
b. destroying the virus-infected host cells (5 ways)
c. protecting uninfected cells from viruses (2 ways)

Back 105

A. i. Opsonization of viruses so they can be destroyed by phagocytes
ii. MAC damage to viral envelope and susequent deactivation of virus
B. i.Opsonization of virus-infected cells so they can be phagocytosed.
ii. ADCC lysis of infected cell by NKs attaching by means of antibodies.
iii. MAC lysis of infected cell by cativation of classical complement pathway by antibodies.
iv. CTL destruction of infected cell showing foreign epitope(most important way)
v. NKs lysis of cells that fail to express MHC-I.
c. i. Virus-neutralization by antiboies coating the virus.
ii. Interferons prompting other cells to destroy mRNA if they become infected, killing themselves and virus.

Front 106

IIB7
* Briefly describe 2 different ways bacteria may resist antibodies that block bacterial adherence to host cells.

Back 106

Some bacteria can degrade IgA with proteases others simply change pili tips or surface proteins so the antibodies can't bind.

Front 107

IIB5
* Discuss how antibodies defend the body by way of neutralizing exotoxins.

Back 107

Antibodies combine with the toxin and neutralize it, preventing its reaction with host cells.

Front 108

IIC2
* List 3 different forms of antigen that may be used for artificially acquired active immunity and state 2 common examples of each.

Back 108

Attenuated microbes (MMR vaccine for against measels, mumps, and rubella; Yellow fever vaccine)
Killed or fragmented microbes or antigens produced by recominant DNA. (Rabies vaccine, Hepatitis B vaccine)
Toxiods, or exotoxin that is treated so as to be nontoxic. (diptheria and tetanus components of DTaP and Td)

Front 109

IIIA
* State three different ways by which cell-mediated immunity protects the body.

Back 109

1. CTLs lyse body cells displaying foreign antigens.
2. Macrophages and NKs destroy intracellular pathogens.
3. Secretion of cytokines that control other cells involved in immunresponces.

Front 110

IIB4
* Discuss how antibodies defend the body by way of ADCC by NK cells.

Back 110

Nks have receptors on surface for Fc part of antibodies. When antibodies have been made aginst antigens on cells, their Fab portion reacts with the antigen and the Fc portion binds to the NK cell, allowing it kill using perforins and granzimes

Front 111

IIB7
* Discuss how antibodies defend the body by way of preventing bacterial adherence to host cells.

Back 111

Antibodies are made agains pili, capsules, and adhesins to prevent bacterial adherance.