T cell receptor and MHC Flashcards

1
Q

primary fn of T cells

A

monitor intracellular env of host cell

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2
Q

TCR is (soluble/transmembrane)? What modification does it have?

A

transmembrane, glycosylated

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3
Q

CD3

A
  • after antigen binds to TCR, CD3 transcribes signal

- cell becomes activated

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4
Q

what do aB TCRs recognize?

A

short peptides generated from antigenic proteins presented by MHC on cell surface

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5
Q

strand with most variability in MHC Class I

A

a1 and a1

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6
Q

strand with most variability in MHC Class II

A

B1

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7
Q

a chain of MHC class II

A

monomorphic

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8
Q

can MHC bind multiple peptides?

A

yes - if they share similar sequences

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9
Q

cross-reactive recognition can explain

A

alloreactivity

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10
Q

what happens with peptide-dominant or MHC-dominant binding of TCR?

A
  • TCR can bind to non-self MHC in peptide dominant
  • TCR can bind wrong peptide in MHC dominant
  • responds as if normal
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11
Q

on what cells is MHC I expressed

A

nucleated cells

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12
Q

on what cells is MHC II expressed

A

professional antigen presenting cells

-subset of hematopoietic and thymic stromal cells

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13
Q

CD4 and CD8 interact with (variable/non-variable) regions of MHC

A

non-variable

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14
Q

CD4 and CD8 act as co-receptors on T cells and increase _____ sensitivity for peptide MHC

A

aBTCR

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15
Q

expression of MHC is

A

codominant

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16
Q

MHC haplotype

A

complete set of alleles within an animal’s MHC

17
Q

are divergent MHC haplotypes good or bad

A

good - allow presentation of more peptides -> more protection

18
Q

2 reasons for diversity of MHC

A
  • polymorphism - allelic variation

- polygeny - several different MHC genes (w/ similar fn)

19
Q

relative risk = 1

A

no increased risk with trait

20
Q

relative risk > 1

A

association between allele and disease

21
Q

relative risk =

A

RR = allele in individuals with disease / allele in individuals w/out disease

22
Q

MHC I presents what kind of pathogen

A

cytosolic

NOT extracellular

23
Q

MHC II presents what kinds of pathogen

A

intravesicular (macrophage), extracellular (B cell)

NOT cytoplasmic

24
Q

what happens when MHC I presents a cytosolic pathogen

A

cell death

25
Q

what happens wheh MHC II presents an intravesicular pathogen on a macrophage

A

macrophage is activated to kill

26
Q

what happens when MHC II presents extracellular pathogens and toxins on a B cell

A

B cell is activated, secretes Ih to eliminate extracell bacteria/toxins

27
Q

how does MHC I process antigen

A
  • peptide is ubi -> fragmented in proteaome
  • peptide binds TAP in ER
  • goes to lumen in ER
  • finds MHC I bidning groove, displaces self peptide
  • MHC I:peptide goes to cell surface
28
Q

how does MHC II process antigen

A
  • antigen ingested -> phagolysosome, degraded by proteases
  • peptides go to endosomal compartments
  • find binding groove of MHC II, displace CLIP
  • MHC II:peptide go to cell surface
29
Q

bridge between TCR and MHC, stimulate high percentage of T cells bearing V genes

A

superantigens

30
Q

what don’t need to be presented by MHC to be antigenic

A

superantigens

31
Q

TSS causes overproduction of

A

IL2, IL4, IL1, TNF-a