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MIMM214 > linking innate to adaptive immunity > Flashcards

linking innate to adaptive immunity Flashcards

1
Q

what are the 3 signals for activation of t cells?

A

1- activation: pMHC:TCR
2- survival: B7.1 or B7.2 / CD80 or CD86 :CD28
3- differentiation: cytokines

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2
Q

what happens with DCs when they encounter PAMPs? (4 things)

A

increase migration receptors expression (ex CCR7)
increases antigen processing
increases costimulatory molecules expression (not present in naive DCs)
increases MHC molecules expression

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2
Q

what happens with DCs when they encounter PAMPs?

A

increase migration receptors expression (ex CCR7)
increases antigen processing
increases costimulatory molecules expression (not present in naive DCs)
increases MHC molecules expression

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3
Q

what is priming?

A

first contact of T cell with their antigen

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4
Q

what are 3 characteristics of unactivated/immature DCs?

A

many dendrites
can phagocytose
located in peripheral tissue

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5
Q

what are characteristics of activated DC in lymphoid tissue?

A

express MHC peptide and costimulatory molecules
interacts with T cell

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6
Q

what are characteristics of conventional DCs?

A

travel to lymphoid tissue once activated
activate T cells in lymphoid tissues
conventional/professional APC

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7
Q

what are characteristics of plasmacytoid DCs?

A

high PRRs levels
can produce large amounts of type I IFN
stay at infection site
secrete cytokines that amplify local response

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8
Q

what happens to T cell once it is activated by DC?

A

proliferation

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9
Q

name 3 types of lymphoid tissues

A

lymph nodes, spleen, peyer’s patch

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10
Q

through what structures do DCs and T & B cells enter and exit lymph nodes?

A

DCs enter via afferent lymphatics
T & B cells enter via high endothelial venules HEV and exit via efferent lymphatics

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11
Q

what happens if antigens from virus kills the DC?

A

DC transfer antigen to resident DC or cDCs

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12
Q

how long do lymphocytes spend in secondary lymphoid organs? why?

A

they spend hours trying to find their antigen match and return to circulation if they don’t

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13
Q

what do T cells become once they are activated and proliferate?

A

effector T cells

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14
Q

where do PRRs get activated?

A

in periphery tissue

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15
Q

what are the 4 stages of T cell entry into the lymph node

A

rolling, activation, adhesion, diapedesis

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16
Q

what are adhesion molecules and chemokines involved in T cell entry in lymph node?

A

selectins
CCL21 (chemokine binding to CCR7)
integrin

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17
Q

what is each adhesion molecule’s role?

A

selectins: rolling adhesion to HEV & targetting to lymphoid tissue
chemokines: activation
integrin: arrest and adhesion

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18
Q

what can DCs secrete to attract T cells?

A

chemokines

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19
Q

what are fibroblastic reticular cells? what can they do?

A

cells that provide roadways for naive T cells and secrete CCL21 chemokines to help attract T cells and DCs to lymph nodes

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20
Q

what happens when T cells find their Ag match?

A

they stop moving and commit to a 8 hours or longer relationship with DC

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21
Q

for how long can T cells experience proliferation and differentiation?

A

for 4 days! what causes inflammed lymph nodes

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22
Q

where do T cells arise from

A

arise in thymus from bone-marrow progenitors

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23
Q

what do T cells recognize?

A

antigen peptide fragments bound to self molecules of MHC

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24
Q

what does MHC stand for and where are they expressed?

A

Major Histocompatibility Complex. expressed on APCs membrane

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25
Q

what do CD stand for

A

clusters of differentiation

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26
Q

what are the 2 types of T cells

A

CD8+ (cytotoxic T lymphocytes)
CD4+ (Helper T cells - TH1, TH2, TH17, Treg, TFH)

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27
Q

what do each type of T cells recognize?

A

CD4+ recognizes Ag on MHC II
CD8+ recognizes Ag on MHC I

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28
Q

what influences what type of effector T cell will arise

A

the PAMP that activated DC which influences the type of cytokines produced -> leads to type of effector T cell

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29
Q

where do DCs get activated?

A

in the lymph nodes

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30
Q

what is CCR7?

A

a chemokine receptor

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31
Q

what tissues have receptors for selectins?

A

HEV and mucosal epithelium

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32
Q

Does T cell - Ag encounter in lymph node always lead to activation?

A

no: sometimes the DC dies or else

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33
Q

what kind of synapses does T cell-APC interaction form?

A

immunological synapse (long-term interaction)

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34
Q

what is contained in the TCR complex?

A

TCR, CD3, zeta chain, and ITAM motifs

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35
Q

what are ITAM motifs and where are they located?

A

Immunoreceptor tyrosine-based activation motif. Located on intracellular chains of CD3 and zeta chain.

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36
Q

When are we going to find clonotypic TCRs?

A

when a TCR gets activated and clones itself (otherwise all TCRs are different)

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37
Q

how can we have so many different adaptive immune receptors (BCRs, TCRs)?

A

DNA rearrangement of variable, diversity, joining, and constant genes

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38
Q

each chain of a TCR has which domains?

A

alpha chain: V, J and C domains
beta chain: V, D, J, and C domains

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39
Q

each domains have so many copies of each except which?

A

there’s only 1 constant region

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40
Q

what are professional APCs?

A

conventional DCs, macrophages, activated B cells

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41
Q

what are professional APC’s characteristics

A

express MHC class I AND class II molecules.
Express costimulatory molecules when activated.

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42
Q

what are non-professional APCs?

A

all cells expressing MHC class I under normal conditions (therefore all nucleated cells)

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43
Q

what type of peptide does each type of MHC present?

A

MHC class I = endogenous peptides (intracellular/cytosolic)
MHC class II = exogenous peptides (extracellular origin)

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44
Q

what is an MHC class I molecule made of?

A

MHC class I = 3 domain big TM alpha chain + 1 non-covalently bond constant beta2 microglobulin

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45
Q

what is an MHC class II molecule made of?

A

TM alpha + TM beta chain that have 2 domains each

46
Q

apart from the alpha and beta chains, what do MHC class I and II require to be expressed stably?

A

peptide

47
Q

what are Ig-like domains? what stabilizes it

A

immunoglobulin-like; domain of aprox 100 aa with alpha helices, beta strands, stabilized by an intrachain disulfide bond

48
Q

what differences are found in MHC’s peptide-binding cleft?

A

allele-specific differences

49
Q

where are IG-like domains found?

A

on each MHC chain

50
Q

what are coreceptors? why are they there?

A

CD4 and CD8 molecules in T cell membrane. attach to MHC constant region to increase affinity of binding
and
initiate TCR signaling (signal 1)

51
Q

what is CD4’s structure?

A

single chain with 4 Ig-like domains

52
Q

where are Ig-like domains found?

A

on each MHC chain (and on CD4 and CD8 chains)

53
Q

how do endogenous pathogens enter the cells?

A

present their HA/NA molecules to cell’s membrane receptors
or
enter with help from CD4 and coreceptor

54
Q

what are proteasomes?

A

protease complexes that degrade polyubiquitinated proteins (antigen peptides) in the cytosol

55
Q

what type of peptides are presented on MHC class I?

A

endogenous peptides and self-peptides

56
Q

what is calnexin?

A

chaperone that holds MHC I alpha chains until beta2 microglobulin binds

57
Q

what chaperones help beta2 microglobulin interact with MHC I alpha chain?

A

calreticulin, ERp57

58
Q

what is TAP?

A

protein bound to MHC I by tapasin that pumps peptide fragments from the cytosol to the ER

59
Q

what is ERAAP function?

A

trims peptides in ER that are too long to bind MHC I

60
Q

what allows MHC to be properly folded?

A

peptide binding to groove

61
Q

what happens once the peptide binds to MHC?

A

pMHC-I is released from TAP and goes to cell membrane

62
Q

where are exogenous peptides fragments generated?

A

from internalized antigens in endocytic vesicles (endosome fused with lysosome)

63
Q

what happens in APCs at the same time as exogenous peptide degradation?

A

production of MHC class II molecules in the ER

64
Q

how are proteases degrading exogenous peptides activated?

A

by acidification of endosome when it fuses with phagosome

65
Q

what is the invariant chain?

A

chain that binds to MHC class II groove to transport it from ER to endocytic vesicle.
also prevents peptides from binding to MHC II too early in the ER.

66
Q

what is CLIP?

A

class-II associated invariant chain peptide: what becomes the invariant chain after it gets degraded by proteases in endocytic compartments

67
Q

what causes the cleavage of li in endocytic vesicles?

A

acid pH

68
Q

what is HLA-DM?

A

Human Leukocyte antigen-DM: releases CLIP from MHC II in endocytic vesicles

69
Q

what is cross-presentation?

A

exogenous antigens are redirected to the endogenous presentation pathway (MHC I)

70
Q

broadly how does cross-presentation work?

A

CD4+ T cells give permission to DC to redirect the exogenous Ag to CD8+ T cells.
DC presents exogenous Ag on MHC I to CD8+ T cells

71
Q

what is required for cross-presentation?

A

activated CD4+ that license DC

72
Q

what is hypothesized to be the “license” in cross-presentation?

A

IL-2 cytokine

73
Q

what are autophagosomes?

A

vesicles that fuse with lysosomes to degrade cytosolic and exogenous peptides and present them to MHC II

74
Q

what is “the digestion and breakdown by a cell of its own organelles and proteins in lysosomes?”

A

autophagy

75
Q

how is T cell response restricted?

A

MHC restriction: T cell can only recognze a specific peptide when it is bound to a specific SELF MHC molecule

76
Q

can an animal of a specific strain respond to an Ag on a different animal’s strain APCs?

A

no

77
Q

what is an allogeneic MHC molecule?

A

a non-self MHC molecule

78
Q

what % of T cells can respond to allogeneic MHC molecules? what is this phenomenon called?

A

1-10%
allorecognition

79
Q

what does allorecognition cause related to grefs/transplants?

A

rejection of transplanted organs

80
Q

what is an allele LOL

A

a specific form of a gene

81
Q

what genes encode MHC molecules? where are they found?

A

HLA (human leukocyte antigen) genes on chromosome 6

82
Q

different HLA genes code for different what?

A

for different MHC class alpha domain!
(ex MHC class I genes include HLA-A, HLA-B, HLA-C, and MHC class II genes include HLA-DR, HLA-DQ, HLA-DP, …)

83
Q

what part of MHC I is not encoded by many alleles?

A

beta 2 microglobulin

84
Q

what is polymorphism vs polygeny?

A

polymorphism: multiple alleles for each gene (ex HLA-A1 and HAL-A581)
polygene: individual has many copies of genes with the same function (ex HLA-A, HLA-B, HLA-C)

85
Q

what is a haplotype in MHC context? how many do we inherit?

A

a particular combination of MHC alleles on a single chromosome. we inherit one from each parent

86
Q

Which inherited MHC genes are expressed in offspring cells? why?

A

one maternal haplotype and one paternal haplotype -> get the most combinations to be able to present the most AGs

87
Q

can there be an organ transplant between siblings?

A

it will probably still be rejected because even siblings

87
Q

can there be an organ transplant between siblings?

A

it will probably still be rejected because even siblings inherit different combinations

88
Q

what makes transplantation difficult?

A

human are heterozygous (except very rare exceptions)

89
Q

how many MHC I alleles do you inherit from each parent?

A

3 (HLA-A, HLA-B, HLA-C)

90
Q

where are the differences between alleles located?

A

on peptide binding groove. In MHC II, usually on the beta chain

91
Q

when is a transplant successful?

A

if the recipient has the allele(s) of the donor

92
Q

what are the two type of receptors we learned about?

A

intrinsic kinase activity
extrinsic kinase activity (kinase is noncovalently associated with the receptor)

93
Q

how do receptors with intrinsic kinase activity work?

A

downstream signaling is initiated by dimerization and transphosphorylation

94
Q

how do receptors with extrinsic kinase activity work?

A

downstream signaling is initated by recruitment of kinase and dimerization, followed by transphosphorylation

95
Q

what is SH2?

A

a domain in receptor that has selective binding properties for phosphorylated tyrosine on other proteins

96
Q

what do phosphorylated tyrosine do?

A

they’re just binding sites for a number of protein-interaction domains

97
Q

how are multimolecular complexes made?

A

can form around adaptor proteins

98
Q

what are phosphatases?

A

proteins that dephosphorylates other proteins

99
Q

what is Lck and what does it do?

A

extrinsic co-receptor-associated kinase that phosphorylates ITAMs in the TCR upon co-receptor binding with Ag:MHC

100
Q

what does phosphorylation of ITAMs trigger?

A

activation of Zap-70 which activates many downstream signaling molecules, leading to TFs

101
Q

what are positive costimulatory receptors?

A

CD28: facilitates activation

102
Q

what are negative costimulatory receptors?

A

CTLA-4, PD-1: help turn off activation for regulation

103
Q

what is an anergic T cell? in what context do we find them?

A

a non responsive T cell. in absence of costimulation

104
Q

what are CD28 characteristics? (3)

A
  • EXTRINSIC TM homodimer glycoprotein
  • present at baseline
  • binds B7.1 and B7.2 (CD80/86) on activated APCs
105
Q

what does CD28 binding to B7 trigger?

A

phosphorylation of CD28 -> recruitment of kinase -> additional signaling

106
Q

why is it good that T cells become anergic?

A

decreases the probability of autoreactive T cells

107
Q

what is caused by signal 1 and 2 on T cells (broadly)

A

IL-2 and IL-2Ralpha transcription -> secretion -> proliferation

108
Q

what is IL-2?

A

an autocrine cytokine that bind on receptor on same cell and induces proliferation signal

109
Q

what type of cell populations come from IL-2 induces proliferation?

A

memory and effector clonal cells

110
Q

what is the other name for IL-2Ralpha? what is it?

A

CD25
it’s a part of the IL-2 receptor

111
Q

what parts of IL-2 receptor is constitutively expressed? can they bind IL-2?

A

IL-2R beta and gamma. they can bind IL-2 but only weakly without IL-2R alpha

MIMM214 (5 decks)

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