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MIMM 214 > T Cells 6 > Flashcards

T Cells 6 Flashcards

1
Q

what happens after T cell activity?

A

contraction and negative regulation of T cells

and restoration of epithelial activity

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2
Q

when does the immune response contract?

A

within 10-14 days of infection –> at the end of the primary immune response, once Ag is cleared

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3
Q

how do Treg cells help with contraction?

A

by releasing inhibitory cytokines

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4
Q

how are lymphocytes lost for clonal contraction?

A

via apoptosis

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5
Q

which types of lymphocytes remain after clonal contraction? what type of response will they be needed for?

A

memory cells –> for secondary response when antigen is encountered again

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6
Q

what are the 2 unknown aspects of clonal contraction?

A
  1. is clonal contraction triggered by a lack of Ag or an active switch?
  2. how are memory cells selected for survival instead of death induction
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7
Q

what are the 2 apoptosis pathways?

A
  1. intrinsic pathway
  2. extrinsic pathway
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8
Q

what is another name for the intrinsic apoptosis pathway? how does the intrinsic pathway work?

A

“death by neglect”

lack of IL2Ralpha expression = absence of IL-2 survival signal = apoptosis

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9
Q

what property of IL-2Ralpha allows the intrinsic pathway to occur? what type of molecules have this common property?

A

IL-2Ralpha has transient expression, so it is impermanent and can therefore be reduced when needed

common for all cytokine receptor expression

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10
Q

what are the 2 types of inhibitory/regulatory receptors?

A
  1. CTLA-4
  2. PD-1
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11
Q

what is the function of CTLA-4?

A

downregulates T cell activation

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12
Q

how does CTLA-4 downregulate T cell activation?

A

binds B7 molecules with higher affinity than CD28, so it sequesters B7 and prevents CD28 binding

ultimately shuts down signaling pathways

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13
Q

when is CTLA-4 induced?

A

after signal 1,2,3 about 24h after T cell activation

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14
Q

when does CTLA-4 activity peak?

A

2-3 days post-stimulation

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15
Q

how does CTLA-4 get expressed on cell membrane?

A

CTLA-4 is fully translated intracellularly but undergoes PHOSPHORYLATION (post-translational regulation)

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16
Q

how many B7 molecules does CD28 bind vs how many B7 molecules does CTLA-4 bind?

A

1 CD28 binds 1 B7

1 CTLA-4 binds 2 B7

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17
Q

describe what happens when effector T cell binds APC (describe without vs with CTLA-4)

A

WITHOUT:
- Effector T cell binds APC
- CD28 can bind B7 and allow proliferation

WITH CTLA-4:
- Effector T cell binds APC
- CTLA-4 binds B7, blocking CD28 and blocking proliferation

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18
Q

ultimately, how does CTLA-4 affect sensitivity of T cells to APCs and how does affect proliferation?

A

CTLA-4 makes activated T cells less sensitive than naive T cells to stimulation by APCs

reduces IL-2 production which reduces proliferation and prevents lymphocyte overgrowth

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19
Q

what happens in mice that don’t have CTLA-4?

A

too many lymphocytes –> disease

20
Q

what cells express PD-1?

A

activated T cells express PD-1

21
Q

What does PD-1 bind? (2)

A
  1. PDL-1
  2. PDL-2
22
Q

what type of cells express PDL-1?

A

constitutively express on many cells

23
Q

what type of cells express PDL-2?

A

on APCs during inflammation

24
Q

what is the function of PD-1?

A

downregulates T cell activation/function

25
Q

what is PD-1 a marker of? when is this common?

A

marker of T cell exhaustion, common in chronic diseases

26
Q

why is PD-1 a marker of exhaustion?

A

if cell gets tired of proliferating, etc. it will “wave a white flag” aka allow PD-1 activity

27
Q

what are the 2 subsets of Treg cells?

A
  1. Natural Treg (nTreg)
  2. Induced/adaptive Treg (iTreg)
28
Q

where do nTregs come from?

A

produced directly in thymus and can exert its function as is

29
Q

when are nTregs selected?

A

have high affinity for self peptides to dampen immune response to them

helps prevent autoimmunity

30
Q

what 5 molecules do nTregs express?

A
  1. TCR
  2. CD4
  3. IL2Ralpha
  4. CTLA-4
  5. FoxP3 (master transcriptional regulator)
31
Q

do nTregs express IL-2?

A

no, so they rely on other cells

32
Q

where do iTregs come from?

A

arise in periphery from CD4+ T cells

33
Q

what 5 molecules do iTregs express?

A
  1. TCR
  2. CD4
  3. IL2Ralpha
  4. CTLA-4
  5. usually FoxP3 (master transcriptional regulator)
34
Q

what are the 4 steps of iTreg signaling?

A
  1. signal 3: IL-2, TGF-beta
  2. TF: STAT5
  3. master transcriptional regulator: FoxP3
  4. secretes IL-10, TGF-beta
35
Q

what effector cytokines do both Treg cell types secrete? what type of cytokines are they?

A

IL-10 and TGF-beta

anti-inflammatory cytokines

36
Q

how do IL-10 and TGF-beta affect immune cells? what specific type of immune cell do they mainly affect?

A

IL-10 and TGF-beta repress immune cells, mainly T cells

37
Q

what are the 4 main functions of Tregs?

A
  1. deplete local area of stimulating cytokines
  2. produce immunosuppressive/anti-inflammatory cytokines
  3. directly kill T cells
  4. inhibit APC activity
38
Q

how do Tregs deplete the local area of stimulating cytokines?

A

express IL-2Ralpha (CD25) to sequester IL-2 and prevent proliferation signal

39
Q

do Tregs make their own IL-2?

A

no, they steal it from other cells and only express IL-2Ralpha

40
Q

what anti-inflammatory cytokines do Tregs produce? what do they do?

A

IL-10 and TGF-beta

stop pro-inflammatory cytokines

41
Q

how do Tregs directly kill T cells? (2)

A
  1. granzymes
  2. metabolic disruption
42
Q

how do Tregs inhibit APC activity? (2)

A
  1. B7 sequestration by CTLA4
  2. endocytose B7 from APCs
43
Q

what are 3 roles of IL-10?

A
  1. inhibits MHC expression from APCs
  2. inhibits B7 expression from APCs
  3. inhibit production of TH1 and TH17 cytokines
44
Q

what are 2 roles of TGF-beta?

A
  1. inhibits T cell proliferation
  2. inhibits development and function of TH1 and TH2
45
Q

where does nTreg arise? why?

A

nTreg arises in thymus –> mainly recognizes self-peptide:MHC

46
Q

where does iTreg arise? why?

A

iTreg arises in periphery –> recognizes self-peptide/Ag peptide:MHC

MIMM 214 (33 decks)

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