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MIMM 314 > Lecture 19 - Memory T Cells > Flashcards

Lecture 19 - Memory T Cells Flashcards

1
Q

2 things that happen when infection gets resolved

A
  1. contraction
  2. memory
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2
Q

what happens during contraction of immune response?

A

apoptosis kills most effector T cells but some cells remain as memory cells

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3
Q

what is AICD?

A

Activation-Induced Cell Death in activated T cells

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3
Q

why does AICD occur?

A

ensures homeostasis so we don’t have accumulation of lymphocytes from each response

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4
Q

what 2 things can trigger AICD

A
  1. Fas-L binding Fas
  2. TNFalpha/beta binding TNFR-1
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5
Q

role of IL2 in AICD

how does this relate to its normal role?

A

promote Fas-FasL dependent AICD on activated T cells

normally IL2 promotes T cell growth

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6
Q

what cells express FasL?

A

effector T cells

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7
Q

wha cells express Fas? what is the form of Fas?

A

activated T cells

Fas is in a trimer

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8
Q

what is the domain on Fas and TNFR-1 that mediate apoptosis

A

cytoplasmic death domains –> caspases 8/3

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9
Q

role of caspases

A

to chop up DNA inducing apoptosis

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10
Q

what happens with mutated Fas and FasL?

A

Leads to lymphoproliferative and autoimmune disorders

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11
Q

what occurs in a successful primary immune response?

A

pathogen is eliminated and there is long-lasting immune memory

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12
Q

besides T cells, what other component of the immune system protects against a re-infection?

A

Abs

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13
Q

how do Abs protect against re-infection?

A

neutralization and opsonization

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14
Q

4 effector functions of memory T cells

A
  1. cytokines
  2. cytotoxicity
  3. help
  4. regulation
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15
Q

how does Ab response change in primary vs secondary response? (2)

A

amount and affinity of Ab increases

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16
Q

lifespan of human memory T cell vs lifespan of human T cell memory

A

memory T cell: 30-160 days

T cell memory: 10-15 years

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17
Q

if T cell memory lasts much longer than a memory T cell, what does this indicate about memory T cells?

A

longevity is not an intrinsic characteristic of circulating memory T cells –> there is self-renewal of specific and highly differentiated/rapid effector functions

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18
Q

in CMV-carrying patient who underwent immunosuppressive treatment, what happens to CD8+ T cells when there is an increase in viral load and then when virus is cleared?

A

increase in viral load = increase in virus-specific effector CD8+ T cells

virus is cleared = 5% of activated T cells become memory T cells

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19
Q

describe relative number of Ag-specific T cells throughout immune response

A

Infection: increase up to 10,000x more Ag-specific T cells than naive

Memory: decrease to 100x more Ag-specific T cells than naive

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20
Q

describe how the relationship btwn number of memory cells and control of infection changes with age

A

young: more memory cells = more control of infection

old: more memory cells does not correlate to control of infection

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21
Q

why does the amount of memory cells not correlate to control of infection?

A

IMMUNOSENESCENCE

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22
Q

what is immunosenescence?

A

function/efficiency of the memory T cells decreases with age

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23
Q

what are 3 things that can cause immunosenescence?

A
  1. genetics
  2. epigenetics
  3. host factors
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24
is it possible for a "new" infection to be mediated mainly by memory T cells? example
yes --> for example, influenza has different antigenic proteins that can make up the virus and individual can be infected with virus that has similar components as one they had previously been infected with
25
what happens if someone is infected with influenza with epitopes A,B,C and then later in life is infected with epitopes B,C,D?
Will have HIGH response to B and C because already previously exposed to them
26
describe competition of memory vs naive T cells
memory T cells compete with naive T cell response to the same antigen --> if memory has been developed, memory will predominate
27
is memory dependent on repeated exposure to infection?
no, the memory for an epitope from 1 infection can be long-lasting
28
how does a memory response change with each infection?
strength declines/weakens
29
if a memory response weakens with each infection, when can a new + strong primary response take over?
at the 5th infection there is no memory response so disease occurs and a new primary response occurs
30
where do T cells migrate? (2)
lymphoid tissues or peripheral tissues
31
describe the differentiation of T cells with increasing antigen exposure (5)
1. Naive T cell 2. Tscm 3. Tcm 4. Tem 5. Teff
32
which types of T cells migrate to lymphoid tissues?
1. naive 2. Tscm 3. Tcm
33
which types of T cells migrate to peripheral tissues?
1. Tem 2. Teff
34
which T cells can become memory cells?
T cells in periphery --> Tem and Teff
35
describe Teff cells and their fate
fully active and differentiated --> end up dying or become tissue-resident memory cells
36
what allows for the migration of T cells to lymphoid tissue or peripheral tissue?
chemokine receptors and adhesion molecules
37
Effector Memory T (Tem) cells - proliferative ability - CCR7? why? - what do they secrete? - where do they migrate?
Tem - not highly proliferative - lack CCR7 bc not LN resident, so they migrate to tissues - secrete IFNy, IL4, IL5, or cytotoxic mediators for CD8+ - migrate to peripheral tissues
38
Central Memory T (Tcm) cells - proliferative ability - CCR7? why? - where do they migrate? - how do they migrate?
Tcm - highly proliferative - express CCR7 bc LN-resident - migrate to LN - L-selectin binding, then CCR7 signaling by SLC (like naive T cells)
39
describe Tem vs Tcm response to pathogens
Tcm gave better protection against viruses, bacteria, and cancer compared to Tem
40
Stem Cell Memory T (Tscm) cells - proliferative ability - role
Tscm - highly proliferative - Tscm is the reservoir of the reservoir: make Tcm and Tem subsets while maintaining themselves
41
Tissue-Resident Memory T cells - movement in body - role - how do they compare to Tcm and Teff cells? (3)
Tissue-Resident Memory T cells - occupy tissues and DO NOT RECIRCULATE - rapid first response against re-infections at surface - transcriptionally + phenotypically + functionally distinct from recirculating Tcm and Teff cells
42
what is tropism of memory population determined by?
adhesion and chemokine receptors expressed by T cells
43
how do circulating Tscm, Tcm, and Tem cells reach the intestines?
migrate in blood, circulating thru the spleen and lungs where they get primed to migrate to intestines
44
where are Trm cells mainly found? (4)
1. skin 2. lungs 3. BM 4. intestines
45
what receptor is associated with LN homing?
CCR7
46
what receptors/molecule are associated with skin homing? (3)
1. CCR4 2. CCR10 3. cutaneous lymphocyte antigen (CLA)
47
what receptor and adhesion molecule are associated with intestine homing (2)?
CCR9 and a4B7 integrin
48
what receptor is associated with lung homing?
CCR6
49
what adhesion molecule is associated with BM homing?
a2B1 integrin
50
similarity btwn function of Tcm and Trm cells
can induce effector mechanisms via IFNy, TNF, and IL2 once activated
51
difference btwn Tcm and Trm in terms of IL2
more IL2 is made in Tcm cells so they can be more proliferative
52
difference btwn Tcm and Trm cytotoxicity
Trm have a small amount of PERFORIN and GRANZYME B at resting state that can be induced to make a lot!!
53
why is it important that Trm cells have some perforin and granzyme B that can be induced to make even more?
they already have preformed mRNA that allows them to be ready to go to induce cytotoxicity
54
describe the purpose of comparing WT mice vs MCH II KO mice upon OVA infection
WT has CD4 and CD8 T cells MHC II KO will only have CD8 T cells therefore, we can test how CD8 responses differ depending on presence/absence of CD4
55
does CD8 T cell memory response rely on CD4 T cells? how do we know?
7 days of OVA infection: - CD8 T cells in WT and KO mice are produced in similar amounts 70 days later, re-infected: - only WT can make CD8 T cells therefore, CD4 is important to sustain CD8 memory response
56
if CD4 T cells influence CD8 T cell memory response, how does this affect vaccine development?
vaccine must stimulate CD4 and CD8 so they can allow for sustained memory response --> CD4 licensing
57
what allows survival of memory T cells?
CYTOKINES --> IL7 and IL15
58
How can we test that cytokines allow for survival of memory T cells?
infect mice with virus --> take out CD8 cells with IL7R and without IL7R Transfer CD8 cells into naive mice and infect with virus - transfer of cells with IL7R caused accumulation of memory CD8
59
what molecule is expressed differentily on naive vs memory CD4 T cells?
CD45
60
How is CD45 differently expressed in naive vs memory CD4 T cells?
CD45 on naive CD4 T cells has certain exons to make longer CD45 isoform CD45 on memory CD4 T cells excises those exons to make shorter CD45 isoform
61
how can you use CD45 to determine if CD4 T cell has seen antigen or not?
look at length of CD45 long = naive short = memory
62
what are the 2 opposing things that must be balanced in immune homeostasis
reactivity/immune activation vs tolerance/immunosuppression
63
describe immune tolerance that develops in pregnancy
- normal individual is tolerant to self-antigens and extended self antigens (microbiome) - when pregnant, become tolerant to some paternal antigens in fetus
64
when do we need peripheral tolerance mechanisms?
some self-reactive T cells escape thymus
65
2 peripheral tolerance mechanisms
1. T cell intrinsic (act directly on the self-reactive T cell) 2. T cell extrinsic (rely on other cells)
66
4 T cell intrinsic mechanisms of peripheral tolerance
1. Ignorance 2. Anergy 3. Phenotypic skewing 4. AICD
67
how does IGNORANCE cause T cell intrinsic mechanisms of peripheral tolerance?
Never sees its antigen --> inaccessible due to cryptic antigen in nucleus or poorly presented to immune system
68
how does ANERGY occur to cause T cell intrinsic mechanisms of peripheral tolerance?
lack of signal 2 or via CTLA4/PD1
69
how does PHENOTYPIC SKEWING cause T cell intrinsic mechanisms of peripheral tolerance?
aka immune deviation T cell interacting with self-Ag may undergo full activation but develop non-pathogenic phenotype (incomplete differentiation)
70
2 T cell EXTRINSIC mechanisms of peripheral tolerance
1. Tolerogenic DCs 2. Treg
71
how do Tolerogenic DCs cause T cell extrinsic mechanisms of peripheral tolerance?
low co-stimulation or DCs that make immunosuppressive cytokines
72
2 ways to use phenotypic skewing as therapy
1. prevent T2 asthmatic response so skew response towards T1 2. prevent T1 autoimmune response so skew response towards T2
73
role of DC in the choice btwn immunity and tolerance
IMMUNITY - DCs exposed to PAMP/DAMP causes upregulation of costimulatory molecules to activate T cells for immune response TOLERANCE - immature or tolerogenic DCs exposed to self-protein and presented to self-reactive T cells, causing LOW expression of costimulatory molecules causes T cell tolerance
74
what do Tregs balance?
Tregs allow for balance in activation and suppression by inducing MORE SUPPRESSION
75
What are 6 cells involved in tolerance vs activation of immune response?
1. NK-T cells 2. CD8 T cells 3. Tr1 4. Th3 5. Foxp3- Treg 6. Foxp3+ Treg
76
5 things that rely on activation of immuntiy
1. vaccines 2. allergens, tumours 3. Pathogens/commensals 4. Transplants 5. Autoimmuntiy
77
3 diseases that rely on suppression of immuntiy by Tregs
NON-IMMUNE DISEASES (inflammation induces disease) 1. AD 2. Atherosclerosis 3. T2D

MIMM 314 (23 decks)

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