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IBI Test I > Cell Signaling > Flashcards

Cell Signaling Flashcards

1
Q

shared gamma common subunit

A

JAK1 & JAK3
STAT5a & STAT5b

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2
Q

cytokines activated gamma common subunit

A

2, 4, 7, 9, 15, 21

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3
Q

shared gp130

A

JAK1, JAK2, & TYK1
STAT3

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4
Q

cytokines activated by shared gp130

A

IL-6, 11, OSMR, LIFR

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5
Q

STAT3 activates what hormones

A

prolactin and growth

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6
Q

CD45

A

immune synapse; negative regulation STAT

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7
Q

SOCS1 inhibits

A

STAT1

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8
Q

SOCS3 inhibits

A

STAT3

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9
Q

a mutation in KIR

A

diables SOCS from downregulating signaling

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10
Q

KIR inhibits JAK by functioning as

A

a psuedo stubstrate

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11
Q

High SOCS1 causes

A

high M2 polarization

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12
Q

High SOCS3 causes

A

high M1 polarization

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13
Q

Ruxolitinib

A

inhibits JAK1 and JAK2

treats myelofibrosis by reducing spleen size

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14
Q

Tofacitinib

A

inhibits JAK 3

interferes with IL4 and IL2 signaling, RA treatment

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15
Q

Myd88 dependent pathway

A

fast, rapid production of inflammatory cytokines

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16
Q

Myd88 independent pathway (TRIF)

A

slow, production of INF-a and INF-b

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17
Q

NFkB activation

A

TLR4 binds LPS –> activates TAP–>TAP phosphorylates IKK complex–> IKK phosphorylates IkB –> NFkB translocates to the nucleus

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18
Q

Proximal T cell signaling

A

MHC presents antigen to TCR
CD45 phosphatase disassociates
Lck associates w/ CD 4 or 8
phosphorylates 10 ITAMs on CD3z
allows Zap70 to dock to zeta
Lck phosphorylates Zap70
Zap70 autophorylates

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19
Q

Distal T cell signaling

A

Zap70 phosphorylates LAT and SLP76
—this activates 4 pathways

  1. PLC-y mediated increases calcium
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20
Q

PLC-y increases

A

calcium and IL-2

**also produces IP3 and DAG7 (required for NFkB activation)

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21
Q

calcium pathway

A

calcium binds to calmodulin
calmodulin binds to calineurin

that whole complex goes and phosphorylates NF-AT
NF-AT translocates to the nucleus to drive IL-2

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22
Q

cyclosporine inhibits

A

NF-AT

suppresses IL-2, no T cells —> graft survival

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23
Q

CTLA4 down regulates T cell activity by

A

outcompeting CD28

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24
Q

PD-1:PDL1/2
BTLA: HVEM
down regulate T cell activity via

A

ITIMs

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25
Q

Pembrolizuab acts as cancer therapy through

A

PD-1

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26
Q

Ipilimuab acts as cancer therapy though

A

CTLA4

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27
Q

T reg cell markers

A

CD4, FOXP3, CD25

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28
Q

Tregs express

A

high CTLA4
TGF-b, IL-10, IL-35

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29
Q

Tregs requires

A

IL-2

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30
Q

mutations in FOXP3 cause

A

IPEX

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31
Q

anergy

A

signal 1 is received, but no costimulatory signal

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32
Q

BCR signaling

A

similar to TCR
bind antigen –> acativated SrC kinases –> ITAMs–>Syk docks at SH2 –> phosphorylates PLC-y –> NF-AT, NFkB, etc

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33
Q

main goal of B cell signaling

A

get B cell ready for terminal differentiation into plasma cell

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34
Q

Arp2/3 provides

A

nucleation site for actin molecules to bind

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35
Q

Arp2/3 dramatically improves

A

actin filament polymerization

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36
Q

Arp complex is used to create the _____ for cell movement

A

actin web

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37
Q

TCR: MCH activation activates:

A

PLCy
VAV

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38
Q

Vav activation leads to

A

actin polymerization and cytoskeletal reorganization

39
Q

Rac

A

lamellpodia

40
Q

Rho

A

stress fibers

41
Q

cdc42

A

filopodia, microspikes

42
Q

Rho Family GTPases are key to

A

topography
formation of immune synapse
cell migration

43
Q

activation by cdc42 by Vav is required for

A

WASp mediated actin filament mucleation by Arp2/3

44
Q

WAS triad

A

recurrent viral infections
eczema
thrombocytopenia

45
Q

WASp pathway

A

TCR activation –> recruitment of cdc42 to GTP binding domain –> orients WAS to signaling platform –> WAS pops open –> stabilized by Fyn –> VCA can bind to Arp2/3 –> actin polymerization

46
Q

classic WAS

A

absent/truncated proteins due to premature terminations

LOF

47
Q

X linked thrombocytopenia WAS

A

mutated, nonfunctional protein due to missense mutation
no autoimmunity

LOF

48
Q

x linked neutropenia WAS

A

uncontrolled actin polymerization
mutation in GTPase binding domain

GOF

49
Q

Proinflammatory cytokines

A

6, 2, 12, 17, 23, TNF-a

50
Q

Anti-inflammatory cytokines

A

IL 4, ,5, 10, 13

51
Q

What cytokine drives Th1 differentiation?

A

IL-12

52
Q

What cytokine drives Th2 differentiation?

A

IL-4

53
Q

What cytokine drive Treg differentiation?

A

TGF-b

54
Q

What cytokine drives T17 differentiation?

A

TGF-b, IL-6 (IL-1, IL-23)

55
Q

IFN-y
STAT4
T-bet

A

Th1

56
Q

IL-4
STAT6
GATA3

A

Th2

57
Q

TGF-b
FOXP3

A

Treg

58
Q

IL-17
STAT3
RORyt

A

Th17

59
Q

When TCR binds to CD80/86 this drives

A

actin filament rearrangement
IL-2 production
NFkB production

60
Q

when CTLA4 binds CD80/86

A

prevents cytoskeletal rearrangement
decreases IL-2
induces apoptosis or anergy

61
Q

STAT binds to

A

GAS

62
Q

what do SH2’s two binding sites do?

A

1 weakly binds phosphotyrosine
1 provides a specific binding site for an amino acid side chain

63
Q

a cell exits G0 and enters

A

G1

64
Q

G1: CD4/6 binds to

A

cyclin D

65
Q

S: CDK2 binds to

A

cyclin E

66
Q

G2: CDK binds to

A

cyclin A

67
Q

M: CDK1 binds to

A

cyclin B

68
Q

what cyclin would be upregulated for multiple rounds of division?

A

D

69
Q

a proinflammatory dual-producing Th17 cell expresses

A

IL-17 and IFN-y

70
Q

a proinflammatory dual-producing Th17 cell has what markers

A

Tbet
RORyt

71
Q

a anti inflammatory dual-producing Th17 cell expresses

A

IL-17 and IL-10

72
Q

a anti inflammatory dual-producing Th17 cell has what markers

A

FOXP3
RORyt

73
Q

keratinocytes express ______ causing a feedback loop with Th17

A

IL-23

74
Q

When a Th17 is in a proinflammatory environment, what cytokine is upregulated?

A

IL-23

75
Q

fibroblasts release _______ after exposure to TNF-a

A

keratinocyte growth factor

76
Q

TYK mutation: Homozygous Pro1104/Pro1104

A

increased risk for inflammatory disease
decreased risk of infection

77
Q

TYK mutation: heterozygous Pro1104/Ala1104

A

lower risk of inflammatory disease
lower risk of infection

78
Q

TYK mutation: homozygous Ala1104/Ala1104

A

very low risk of inflammatory disease
very high risk of infection (TB)

79
Q

How innate cells activate adaptive

A
  1. MHC-TCR
  2. CD28 engagement
  3. cytokine activation
80
Q

where does priming of the adaptive immune cells occur?

A

secondary lymphoid organs
thymus spleen lymph node

81
Q

Th1 cells protect against

A

viruses

82
Q

Th2 cell protect against

A

helmiths

83
Q

Th17 cells protect against

A

extracellular toxins, bacteria, fungi

84
Q

Treg

A

anti-inflammatory

85
Q

Why is IL-23 bad for IBD?

A

created a positive feedback loop into Th17

86
Q

SNPs that affect Th17

A

IL23R
STAT3
JAK2
TYK

87
Q

phosphotases turn signaling

A

off

88
Q

Why is Th17 proliferation a good thing?

A

Seals barrier

89
Q

why is diet thought to play a role in Th17 regulation?

A

RORyt

**mechanism unknown but regulates something with fatty acids/cholesterol, ratio gets out of whack, activates RORyt –> Th17 activation

90
Q

a mutation in SH2 causes

A

loss of RTK binding

91
Q

why don’t STAT inhibitors work?

A

the STAT family can heterodimerize, other STATs will fill in

92
Q

JAK inhibs induce

A

anergy, no cytokine signaling

93
Q

CD154

A

aka CD40/CD40L

94
Q

a mutation in Zap 70 would cause

A

no granzymes to be expressed

IBI Test I (18 decks)

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