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Flashcards in Immunology Concepts Deck (34):
1

three phases of autoimmune disease pathogenesis

induction, inflammatory, destructive phases

2

elimination of auto reactive t cells

when immature t cells encounter a high affinity Ag-MHC complex for their TCR, they are deleted in the thymus or periphery

3

signal 1

specific recognition of Ag/MCH complex by TCR

4

Signal 2

co-stimulation via CD28 on T cell with APC CD80/86

5

T cell inactivation/anergy

occurs when T cells encounter signal 1 without signal 2

6

inhibitory co-receptor on T cells that binds to CD80/86

CTLA4

7

how can tolerance be broken?

defective thymic deletion, aberrant help and lack of normal regulation

8

mechanisms for loss of tolerance

defective apoptosis in thymus, immunization with auto antigen, exposure to cross reactive antigens, lack of normal regulation/supression

9

Fas mutation

no apoptosis in the thymus=no selection or tolerance induction. clinically: lymphoproliferation, autoantibodies, nephritis, arthritis

10

how many hyper variable regions do antibodies have?

6

11

function of hyper variable regions on antibodies?

antigen binding (specificity)

12

heavy chain antibody rearrangement

VDJ

13

light chain antibody rearrangement

VJ

14

how many antibody hyper variable loops does it take to bind an antigen?

just 1

15

cross reactivity

other antigens may fit the same antibody, either with similar shapes or by binding in a different way (6 hyper variable loops but only 1 needed)

16

molecular mimicry

when a external antigen looks like an auto antigen. can bypass tolerance.

17

how do autoantibodies cause cellular damage?

they bind to cell receptors and can either initiate abnormal cell activation or prevent normal ligand binding. or they can form immune complexes when bound to soluble antigens (deposit in vessels, complement activation).

18

serum sickness

immune complex mediated disease caused by immunization with a foreign protein can elicit

19

HLA alleles

associated with certain rheumatic diseases

20

how do MHC molecules bind to peptides?

either by binding the peptide backbone (class 2, plasticity) or through the use of specificity pockets (class 1, semi-specificity). both classes do both.

21

MHC1 pathway

endogenous. antigen is synthesized within a cell, degraded by ER, and associated with MHC1 on cells surface to be recognized by CD8 T cell

22

MHC2 pathway

exogenous. endocytosed antigen is degraded by endosome and peptides are associated with HC2 on surface of APC to be recognized by CD4 t cell.

23

TH2 cell

induced via IL4. secretes IL4. defense against parasitic worms, allergy, asthma

24

TH1 cell

induced via IL12. secretes IFNgamma. defense against intracellular pathogens

25

TH17 cell

induced by TGFb & IL6, secretes IL17, defense against extracellular bacteria, AUTOIMMUNITY, cancer

26

Treg

induced by TGFb, secretes TGFb, immunosuppression

27

epitope spreading

stems from the ability of a single activated APC to present multiple antigens. normal. additional t cells may become activated when antigens are complexed together.

28

Autoantigens in RA

T cell immunity to cartilage auto antigens (Type 2 collagen, aggrecan, HC gp39), ubiquitous BiP from the ER, Rheumatoid factor, citrullinated peptide and protein antibodies

29

rheumatoid factor

IgM anti-IgG. enhances the antigen presentation of immune complexes, may have regulatory role

30

citrullinated protein/peptide antibodies

bind to synovial lining cells, fibrinogen, collagen type 1. more likely than rheumatoid factor to be pathogenic.

31

non HLA genes linked to rheumatoid disease

all regulate NO production. their mutations are thought to be a consequence of natural selection against TB. so when we treat patients with anti-TNF therapy, need to be mindful of TB reemergence

32

environmental triggers of RA (combined with HLA DR allele)

smoking, coffee drinking, oral contraception (oxidative stresses)

33

how does oxidative stress possibly lead to RA?

results in protein mutation --> increased protein citrullination --> anti-citrullinated protein antibody generation

34

which antibodies are indicative of lupus?

anti-nuclear antibodies (ANA)