Test 4 Study Guide Part 7

Question 1

Coreceptors:

• Helper T-cells have which coreceptor?
• How does this effect them?
• Cytotoxic T-cells have which coreceptor?
• How does this effect them?

Answer 1

• Helper T-cells have which coreceptor?
  CD4
• How does this effect them?
  can only be activated by MHC-2 presenting cells
• Cytotoxic T-cells have which coreceptor?
  CD8
• How does this effect them?
  Can only kill MHC-1 antigen presenting cells

Question 2

What happens after T Helper cell activation by binding with a MH2?
- What molecule effects cytotoxic t-cells?

Answer 2

Turn into effective Th1, Th2 or other specialties.
B-cell differentiation into plasma cell
cytotoxic T-cell proliferation
- What molecule effects cytotoxic t-cells?
(interleukin-2)

Question 3

FAS:

• Stands for?
• FASL and FAS?
• Where will FASL be found?

Answer 3

• Stands for?
  First Apoptosis Signal
• FASL and FAS?
  FAS receptor on T-cells, FAS ligand activates FAS and causes apoptosis
• Where will FASL be found?
  In a few days into infection T - cells make FASL to kill themselves
  Immune privileged sites (Eye, testes)

Question 4

Mechanisms to defend the testes:

Answer 4

Sertoli cells have tight gap junctions.

Sertoli cells produce FASL

Question 5

Mechanisms to defend the anterior chamber of the eye:

Answer 5

Coating of interior of the eye with FasL

Secretion of different cytokines which inhibit inflammation

Question 6

How do tumor cells use FasL?

Answer 6

Not all but some produce it to protect them from the immune cells by triggering apoptosis of lymphocytes

Question 7

Severe Combined Immunodeficiency Disease:

• other name?
• Cause of disorder:
• Define:

Answer 7

• other name?
  Bubble boy disease
• Cause of disorder:
  inherited, WBC stem cells lack adenosine deaminase
• Define:
  Lack antibody-mediated and cell-mediated immunity

Question 8

Adenosine deamanise is involved in what condition?

Answer 8

A lack of this causes Severe Combined Immunodeficiency Disease

Question 9

Treatment for Severe Combined Immunodeficiency Disease:

Answer 9

Gene therapy with retrovirus.

- many developed leukemia

Question 10

Infection with one disease protects from another closely related one

Answer 10

Cross reactive immunity:

Question 11

Edward Jenner and cow pox (vaccinia) vaccine:

Answer 11

Milk maid exposed to cowpox -> immunity to small pox

Question 12

Edward Jenner and cow pox (vaccinia) vaccine:

Answer 12

Milk maid exposed to cowpox -> immunity to small pox

Innoculate orphan with vaccinia (cow pox) -> infect small pox -> protected orphan

Question 13

Louis Pasteur anthrax vaccine:

Answer 13

Heated anthrax -> lost virulence (attenuated), antigenicity maintained -> inoculated sheep -> they survived

Question 14

Four types of adaptive immunity:

Answer 14

Naturally acquired active immunity
Naturally acquired passive immunity
Artificially acquired active immunity
Artificially acquired passive immunity

Question 15

Naturally acquired active immunity:

Answer 15

Get infected and recover

Question 16

Naturally acquired passive immunity:

Answer 16

Placenta: IgG transfer into plasma

Breast Feeding: IgA and some IgG into gastrointestinal tract (does not enter circulation from GI tract!)

Question 17

Artificially acquired active immunity:

Answer 17

Vaccination

Question 18

Artificially acquired passive immunity:

Answer 18

Gamma globulin shots (IgG injection)
Intravenous immunoglobulin
Antiserum/antitoxin (target and neutralize a toxin)
Antivenom shots (antitoxin)
RhoGam (Rh system, antibodies against big D antigen)

Question 19

Response time:

• Primary response:
• Secondary response:

Answer 19

• Primary response:
  5 - 10 days
• Secondary response:
  ~ 2 hours

Question 20

Secondary response is dependent on what?

Answer 20

Memory B cells
Memory T cells (lesser extent?)
NOT CAUSED BY RESIDUAL ANTIBODIES, exists without them

Question 21

• B- cells inherent there specificity in a massive library
• Each B cell produces one of these antigen options
• When the B-cell finds the antigen it is specific for, it multiplies
• These progeny/clones become plasma cells and memory cells, which respond to infection

Answer 21

Clonal Selection Theory:

Question 22

What are the most abundant lymphocytes in adult?

When do these lymphocytes reduce in levels?

Answer 22

Long-lived T cells of different subtypes, specific for the antigen that caused their generation
About age 70

Question 23

Germinal centers:

- Formation:

Answer 23

• Formation:

B-cell is activated, becomes the center of a massive dividing group of clones, both b memory cells and plasma cells

Question 24

Advantages of germinal centers:

Answer 24

Somatic hypermutation occurs here
Plasma cells are longer lived
Plasma cells have faster replication
Plasma cells have better antibody production

Question 25

Somatic hypermutation:

Answer 25

Occurs in germinal centers. An activated B cell has a higher mutation rate as it continues to divide. This results in plasma cells which make antibodies which are either slightly more or less effective against the invader

Question 26

Vacca:

Answer 26

Latin for cow. | Start of vaccination because of cow pox

Question 27

Salk vaccine:

Answer 27

1st polio vaccine inactivated virus - Only inactivated salk type vaccines are used in the US

Question 28

Sabin vaccine:

Answer 28

Oral live attenuated polio vaccine. Caused about 100 polio cases a year in the US, but is no longer used

Question 29

Three ways to make a vaccine:

Answer 29

- Live viruses (attenuated virulence): - Killed virulent viruses: - Recombinant viral proteins

Question 30

Adjuvants: | - How do they work?

Answer 30

Act as PAMPs or DAMP to bind to pathogen recognition receptors of dendrites. Enhances adaptive immune response. Therefore enhances vaccine 'strength'

Question 31

Fetal self recognition:

Answer 31

Fetus originally capable of targeting self antigens. | Continuous exposure early in fetal and postnatal life results in toleration of an antigen

Question 32

Antibodies targeting the body are called? | T-cells targeting the body are called?

Answer 32

Autoantibodies | Autoreactive T cells

Question 33

Mechanisms of self-antigen removal:

Answer 33

- Clonal Deletion: lymphocytes recognizing self-antigens are destroyed - Clonal Anergy: lymphocytes recognizing self-antigens are prevented from becoming inactive (regulatory t cells)

Question 34

Thyroid gland: - Imune privilege status? - Protein that is hidden self antigen:

Answer 34

- Imune privilege status? Immune privileged - Protein that is hidden self antigen: Thyroglobulin

Question 35

Central Tolerance: - Define: - Controlled by:

Answer 35

- Define: Regulation of potential self targeting lymphocytes in thymus or bone marrow. - Controlled by: Apoptosis, clonal deletion, or anergy

Question 36

Peripheral Tolerance: - Define: - Controlled by:

Answer 36

- Define: Regulation of potential self targeting lymphocytes outside thymus or bone marrow. - Controlled by: Anergy (provided partly by regulatory T lymphocytes)

Question 37

Forbidden clones:

Answer 37

Auto-reactive T Cells, which are kept in check by regulatory T cells.

Question 38

Person's ability to develop active immunity is called:

Answer 38

Immunological competence

Question 39

Immunological competence: - When does it occur? - What helps in the meantime? - What might happen if immune competence occurred in utero?

Answer 39

- When does it occur? ~1 month post-parturition - What helps in the meantime? Passive immunity from IgG that crosses the placental - What might happen if immune competence occurred in utero? Fetus could target mom

Question 40

The fetus is immune to the same antigens as the ____: | How long is breast feeding recommended?

Answer 40

Mother | Exclusively breast milk for 6 months at least (then it can continue)

Question 41

Intravenous immunoglobulin: - Source: - Example of: - Treats:

Answer 41

- Source: Pooled plasma from thousands of people. - Example of: Artificial passive immunity - Treats: First used: combat microbial infections in immunodeficient individuals Now used: Treat autoimmune conditions, immuno-comprimised cancer patients

Question 42

Polyclonal antibody: - What is it? - Why/how is it made?

Answer 42

- What is it? Antibodies in a variety of specificities, some of which have optimal specificity, others of which have poorer specificity - Why/how is it made? Due to somatic hypermutation activated B cells undergoing clonal expansion will produce slightly modified forms. Some with higher affinity and some with low. Polyclonal antibodies include all of these.

Question 43

Monoclonal antibodies: - What is it? - Three letter designation: - Why/how is it made?

Answer 43

- What is it? Pure antibody with optimal antigenic specificity - Three letter designation: MAB - Why/how is it made? Myeloma and plasma cell -> fused -> form hybridoma -> immortalized cell line producing monoclonal antibody

Question 44

Hybridoma:

Answer 44

Immortalized plasma b cell for antibody production. Made by: - myeloma (cancerous cell) fused with plasma B cell

Question 45

``` - Define: monoclonal antibody against HER2 receptors of invasive breast cancers - Treats: invasive breast cancers - Is a type of: Artificially acquired passive immunity ```

Answer 45

Herceptin: - Define: - Treats: - Is a type of:

Question 46

Avastin: - Define: - Treats: - Is a type of:

Answer 46

``` - Define: monoclonal antibody which block VEGF (vascular endothelial growth factor) from binding to its receptors - Treats: Cancer. Colorectal, lung, kidney, brain. - Is a type of: Artificially acquired passive immunity ```

Question 47

Natural Killer Cells: - Target: - Mechanism of action: - Inhibitory receptors:

Answer 47

- Target: Cancer/virus ( - Mechanism of action: (receptor recognition mechanism unexplained, but does not use MHC) Cell-mediated (perforins and granzymes) Destroy on sight, no delay for verification - Inhibitory receptors: MHC inhibits them, stopping them from killing normal host cells.

Question 48

How do NKCs get reinforcements?

Answer 48

Cytokine release to bring in acquired immune cells

Question 49

Three categories of disease of the immune system:

Answer 49

Autoimmune diseases Immune complex disease Allergy (hypersensitivity)

Question 50

Who gets autoimmune diseases more often? | - Why?

Answer 50

Women 2x as likely as in men - Why? Andy thinks its from escaped fetal cells

Question 51

Six reasons for the failure of self tolerance:

Answer 51

1: Immune system exposed to antigen not normally in circulation 2: Self-antigen combines with foreign antigen (or hapten) altering it 3: Antibodies against other antibodies 4: Antibodies produced against foreign antigens may cross-react with self-antigens. 5: Self antigens may be presented with MHC-2 complexes to helper T lymphocytes 6: Inadequate activity of regulatory (suppressor) T lymphocytes