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Immunlogy > TCRs > Flashcards

TCRs Flashcards

1
Q

What is the primary function of TCs?

A
  • To monitor the INTRACELLULAR environment of the host cell

- Exist to help the body evade/deal w/ pathogens

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2
Q

What are CD4+ and CD8+ T cells functions?

A

cd8-target virus infected cell
cd4- function in two types of immunity
1. interacting w/ MO leading to activation–>activation of cytokines
2. help BCs (in form of cytokines) to `differentiate into PC–>production of speciaized Abs

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3
Q

Ways TCR similar to BCR

A
  • contains 1 Ag binding site (2 in Abs)

- contain variable and constant regions

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4
Q

Ways TCR different to BCR

A
  • Where expressed
  • Ag that is recognized
  • Affinity of Ab for Ag much higher
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5
Q

TCR biochemical characterizations

A
  • disulfide linked dimer
  • both chain glycoproteins
  • transmem protein ONLY (no sluable form, unlike Ig)
  • constant and variable region
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6
Q

How is CD3 involved in TCR?

A

TCR alpha/beta chains need help of CD3 molecule to make it to surface

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7
Q

CD3

A

2 pairs of them (4 total) form the TCR complex which escorts TCR A/B chain to surface of cell and is responsible for SIGNAL TRANSDUCTION (ST)
-Cytoplasmic tails of TCR to short to tranduce signal
Once Ag bound to TCR there is ST by CD3 to cell–>Activates cell

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8
Q

Organization/Rearrangement of TCR genes

A

Organized similar to Ig molecule

  • Alpha –>V and J
  • Beta –> V, D, and J
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9
Q

Generating diverse repertoire of TCR

A
  1. recombination of diff gene segments
  2. recombination of diff # of gene segments
  3. Imprecise joining of gene segments
  4. P and N addition
  5. Assembly of diff combination of rearranged TCR chains
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10
Q

What differs TCR in way it generates diversity?

A

Unlike Ig genes, SOMATIC HYPERMUTATION does not occur - (no increase in affinity for Ag)

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11
Q

Which has greater diversity TCR or BCR?

A

TCR

-Alpha has no D regions (like in Ig light chain) BUT has many J regions that contribute to its high diversity

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12
Q

Why is this high diversity important?

A

So TCR can recognize peptide from any Ag it might encounter (since does not undergo somatic hypermutation)

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13
Q

How do BCR and TCR recognize Ag?

A

BCR - recognize structure (naive Ag)

TCR - recognize short peptide fragments presented by MHC molecules

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14
Q

How does affinity for Ag compare?

A

TCR - have weak affinity for peptide/MHC

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15
Q

MHC job?

A

Present Ag

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16
Q

MHC class 1

A
  • alpha chain non-covalently attached to beta 2 microglobulin (stabilizes alpha chain)
  • alpha 3 more constant
  • alpha 1 and 2 form groove for variable part of MHC C1
  • ->w/in groove are residues required to contact peptide
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17
Q

MHC class 2

A
  • have alpha and beta chain
  • most polymorphism in beta 1 domain (alpha 1 monomorphic)
  • grooved formed by beta 1 and alpha 1
  • ->groove contains specific residues for peptide contact
18
Q

Can single MHC molecule bind multiple peptides?

A

Yes, if they share certain sequences

19
Q

How does MHC restrict presentation of Ag on T-cells?

A

TCR can ONLY recognize AG when presented as peptide from MHC molecule

20
Q

Process of restriction presentation

A
  1. APC presents peptide to TCR and CD3 sends signal to activate cell
  2. If have same Ag, but presented on FOREIGN MHC- TCR wont recognize MHC and no activation
  3. Self MHC w/ diff Ag being presented - no activation
21
Q

Alloreactivity

A

Strong TC response to foreign MHC (caused by transplant rejection)

22
Q

Expression of MHC 1

A

Expressed by ALL nucleated cells

23
Q

Expression of

MHC 2

A

Expressed on a SUBSET of hematopoietic cells that are APC and thymic stromal cells

24
Q

Function od CD4 and CD8 om TCs?

A

Function as co-receptors

–increasing alpha/beta TCR sensitivity for peptide MHC

25
Q

Where do CD4/8 cells interact on MHC?

A

On NON-VARIABLE REGIONS

  • MHC 1–> CD8 on CD8+ TCs will react w/ more constant region (alpha 3)
  • MHC C2–> CD$ on CD4+ TCs will interact with non-polymorphic beta 2
26
Q

How do some TCRs recognize presented Ag differently?

A

Some do NOT require Ag to be presented (gamma/delta)

  • can see MHC by itself
  • or bind directly to native Ag
27
Q

MHC haplotype

A

Complete set of alleles found w/in an animals MHC

28
Q

Where do MHC alleles come from?

A

One from each parent

-expressed co-dominantly

29
Q

How does increase diversity between MHC haplotypes help?

A

More divergent haplotypes will present more peptides from any pathogen than more related haplotypes

30
Q

MHC diversity caused by? (2)

A
  • Polymorphism due to allele variation

- Polygeny due to the fact that there are several diff MHC genes w/ similar functions

31
Q

Why is MHC diversity important to survival of HIV?

A

More polymorphism - longer time from serocenversion to live

32
Q

Relative Risk of specific MHC type

A

Look for expression of particular MHC allele w/ and w/o in individuals w/ disease and compare it to those individuals w / and w/o allele

  • no association when = 1
  • > 1 = allele associated w/ disease
33
Q

Where do peptides presented by MHC 1 come from?

A

From cytosolic pathogens or self-proteins in cytosol

-present to CD8+ T-cell–>kill presenting cell

34
Q

Where do peptides presented by MHC 2 come from?

A

Peptides derived from intravesicular pathogens or extracellular pathogens that are taken in
-present to CD4+ T-cells–>kill pathogen or activate B-cells

35
Q

How does MHC class 1 process Ag?

A

Newly syn proteins in CYTOSOL Ub and fragemented into peptides by PROTEOSOME

  • peptides associated with TAP and move to mem of ER and then to lumen
  • peptide placed in binding groove of MHC C1
  • peptide complex goes to cell surface
36
Q

How does MHC class 2 process Ag?

A

Ag ingested and fragmented by PROTEASES

  • peptides move into endosomal compartments and are placed in binding groove on MHC C2
  • displace CLIP (usually in groove to prevent` self-binding of peptides) and goes to surface
37
Q

Cross-presentation of Ags?

A

MHC C1 can express exogenous Ags (where it usually present cytosolic)
MHC C2 can present cellular Ags (where it usually presents extracellular ones)

38
Q

What are SUPERAGs?

A

Act as bridge btween TCR and MHC and stimulate TCs

-DO NOT NEED REC OF PEPTIDE

39
Q

Comparison of SuperAg and Conventional Ag

A
  • Higher freq of responsive T-cells (SA)
  • SA are not MHC restricted
  • SA does not require processing
  • SA does not bind to peptide groove of MHC
40
Q

Ex of superAg?

A

TSST-1 –> Causes toxic shock syndrome since by allowing TCR to bind to MHC

  • causes overproduction of cytokines
  • complications occur
  • death

Immunlogy (15 decks)

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