Autoimmunity 2 Flashcards

1
Q

Name the 5 main functional classes of cytokines.

A
  1. mediate innate immunity 2. regulate lymphocytes 3. activate inflammatory cells 4. affect leukocyte movement 5. Stimulate hematopoiesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the action of IL-12?

A

initiates the TH1 pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the action of IL-4?

A

initiates the TH2 pathway recruits eosinophils and promotes IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is th action of IL-17?

A

initates TH17 pathway and recuriting neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the action of TGF-B?

A

down-regulates the immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the action of IL-5?

A

activates eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What important proteins are encoded on chromosome 6?

A

chromosome 6 encode MHC/HLA proteins (class I and II invovled in antigen presentation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the location and structure of class I MHC.

A

present on all nucleated cells and platelets, consist of a polymorphic a-chain linked to B2-microglobulin (loci HLA-A,B and C) and function to display all proteins made in the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do class MHC I cells interact with other cells?

A

CD8+ cells are class MHC I restricted and NK cells kill cells with abnormal or low class I MHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the location and structure of class II MHC.

A

present on APCs, coded by HLA D (DP, DQ and DR) polymorphic a and B chains bind antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of cells do MHC II class interact with?

A

CD4+ helper T-cells ar class II MHC restricted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name 4 diseases that show a strong association with specifc HLA molecules

A

ankylosing spondylitis (HLA B27), rheumatoid arthritis (DR4), hereditary hemochromatosis (HLA-A), 21-hydroxylase deficiency (HLSBw47)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List the 4 broad headings of autoimmune disorders.

A

hypersensitivity reactions, autoimmune diseases, immune deficiency, amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What 3 general catagories of substances can trigger a hypersensitivity repsonse?

A

exogenous antigens, homologous substances and autologous substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the cause and result of a type I hypersentivity?

A

cause: antigen binds and cross links bound IgE on mast cells; results in variable rxn between hives and anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the 2 phases of type I hypersensitivity.

A

phase 1 is the immediate release of histamine that cuases vasodilation, edema and SM contraction; phase 2 cytokine release occurs 2-24hrs with infiltrate of eos, polys, basos and CD4+ which often cause tissue damage

17
Q

Explain the steps in the activation and degranulation of mast cells.

A

mast cells express Fc receptors that can bind IgE, antigen binds two adjacent surface IgE antibodies, cross linking activates the cell and causes degranulation

18
Q

Contrast primary and secondary mediators released in a type I hypersensitivity rxn.

A

primary: histamine, proteases, chemotactic factors ; secondary: cytokines and products of membrane phopholipids

19
Q

Besides cross linked IgE, name 5 stimui hat can act as mast cell activators.

A

complement anaphylatoxins (C5a/C3a), macrophage derived cytokines (IL-8), drugs (codeine/morphine), bee venom, physical stimuli (heat, cold, sunlight)

20
Q

Describe the sensitization process that mast cells undergo during first antigen exposure.

A

APC present the antigen to CD4+ cell which causes cytokine release and TH differentiation of that T cell to TH2, these cells produce more cyotkines driving the type 1 rxn (IL-4 IgE, TH2 devo; IL-5 eos; IL-13 IgE)

21
Q

What are the most fatal parts of anaphylactic shock?

A

laryngeal edema, bronchoconstriction, drop in BP

22
Q

What mediates a type II hypersensitivity rxn?

A

antibodies

23
Q

Summarize the classes of antibodies using MADGE.

A

IgM (Macro), IgA (malt-mucousal), IgD (surface of na•ve B-cells), IgG (gestation) IgE (eosinophil- AAA)

24
Q

Name the 4 major mechanisms of type II hypersensitivity.

A

opsonization/phagocytosis, ADCC, complement/Fc mediated inflammation and antibody mediated cellular dysfunction

25
Q

What are the mediator and effector cell types in a type II hypersensitivty reaction?

A

mediator: plasma cell produces antibody, effector: complement proteins and phagocytic cells

26
Q

Describe the process of antibody-dependent cellular cytotoxicity.

A

effector cells (with Fc receptor) kill target cells with IgG on the surface (does not invovle phagocytosis ro complement)

27
Q

Give several examples of type II hypersensitivity reactions.

A

transfusion rxns. Erythroblastosis fetalis, autoimmune hemolytic anemia

28
Q

What is the basis of complement and Fc mediated inflammation (type II hypersensitivity)?

A

antibodies are deposited in the extracellular tissues/matrix and IgG of IgM activate the complement causing inflammation (ie. Good pasture Syndrome where basement membrane is the target)