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Immunology > Cytokines, receptors and signaling > Flashcards

Cytokines, receptors and signaling Flashcards

1
Q

these are heritable and each cell in body expresses same one

A

germline encoded

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2
Q

PRR, cytokine receptors and MHC are examples of

A

germline encoded

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3
Q

BCR and TCR are examples of

A

somatic recombination

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4
Q

these are mediated by cytokines and act in paracrine/endocrine or autocrine manner

A

cell contact independent

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5
Q

these occur and are located in 2nd lymphoid organs, allow for increased contact time and interaction

A

cell contact dependent

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6
Q

Pathogens have or make these so PRRs recognize them

A

PAMPs

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7
Q

PRR recognize ______ and are part of which immunity branch

A

PAMP

innate

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8
Q

TLR and Nod are expamples of

A

PRR’s

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9
Q

TLR can recognize ____ and _____ PAMPS

A

cell contact depent or indepent PAMPS

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10
Q

One PRR:PAMP comes into contact, we get

A

intracell signal cascade foor pro-inflamatories regardless if PAMP is attached or unattached to pathogen

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11
Q

Membrane PRRs recruite adaptor proteins that…

A

activate NFkB path to make more pro-inflmamatories

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12
Q

What three cytokines are secreated downstream of NFkB?

A

TNF-a, IL-1 and IL-6

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13
Q

this guy will activate inflammation, neutrophil activation, cause fever in hypothal, APP of liver

A

TNF alpha

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14
Q

TNF-a made by

A

macrophages and T cells

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15
Q

IL-1 does:

A

activates inflamation
causes fever
causes liver synthesis of Acute phase proteins

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16
Q

IL-1 released by

A

macrophages, endothelial cells and so epi

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17
Q

IL-6 causes

A

liver to make acute phast proteins

Cause B CELL TO PROLIFERATE ANTIBODY PRODUCING CELLS

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18
Q

IL-6 gives us a mix of…

A

antB secreating B cells via causing proliferation

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19
Q

what 2 cytokines cause fever

A

TNF-a and IL-1

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20
Q

what do G-CSF and GM-CSF do

A

induce proliferation in bone marrow; egress of PMS from bone marrow during neutrophil influx

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21
Q

induce proliferation in bone marrow; egress of PMS from bone marrow during neutrophil influx

A

granulocyte and granulomonocyte colony stim factor

G-CSF and GM-CSF

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22
Q

where do G-CSF and GM-CSF come from

A

macrophages mostly and Theper and secreated at sight of infection

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23
Q

This is causes ciruculating PMNS (chemotactic)

A

IL-8

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24
Q

IL-8 is really great

A

at triggering leukocytes

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25
Q

IL-8 made by

A

macrophages, endothelial cells, ep cells

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26
Q

Chemokines are good at

A

cauusing leukocytes to hhave increased integrin affinity, chemotaxis or activation of stuff

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27
Q

How are chemokines classified

A

based on number and location of N-terminal cysteine residues

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28
Q

CC, CXC, C and CX3C are secreated by ______ to promote migration of ______ to infectedsites

A

macrophates (or other epithelial/endothelial cells)

PMNS to site of infecion

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29
Q

Chemokines are cell contact dependend/independent

A

INDEPENDENT

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30
Q

Chemokines promote four stages of PMN extravasation

A
  1. rolling
  2. integrine activation by chemokines
  3. stable adhesion
  4. migration through endothelium
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31
Q

T cell activation requires contact ind/dependend

A

DEPENDENT

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32
Q

T cell activation is mediated by VDJ, VJ or both

A

both, needs both alpha and betta chain to function as a receptor

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33
Q

MHC, CD28, CD80 and CD86 are all exaples of

A

germline genes the T cell needs to get activated

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34
Q

CD28 on T cell binds to

A

B7 on APC

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35
Q

T cell expression of CTLA-4 results int

A

negatively regulating activation and competes with B7 to provide a ‘stop’ signal by binding to CD28

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36
Q

CTLA-4 are ____inflamatory and are contact dependent/indepentdent

A

ANTI inflammator

DEPENDENT

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37
Q

negatively regulating activation and competes with B7 to provide a ‘stop’ signal by binding to CD28

A

CTLA-4

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38
Q

Once TCR binds it will upregulate expression of:

A

CD40L expression (for B cell Ig class switching)
IL2 and IL12 receptor
DNA synthesis of NFAT and NFkB

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39
Q

Why does TCR upregulate CD40L once activated

A

key for B cell Ig class switching

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40
Q

cytokine that provides autocrine cell-contact INDEPENDENT, pro-proliferative feeback to Th cell producing it

A

IL-2

41
Q

Why does TCell upregulate IL2-R once activead

A

because it will also release IL-2 once activated and IL-2–IL-R will cause pro-proliferaction…. autofeedback

42
Q

This is directed by several cell-contact IND. signals produced by both APCs and Th cells themselves

A

Th cell differenctiation

43
Q

APC–> IL-12 to promote Th1 expression of

A

IFN-gmma

44
Q

IL-12 and IFN-gmma cause Th–>

A

Th1

45
Q

TGFB makes by lots of cell types and cauaes induction to Th–>

A

Tregs (Th17)

46
Q

IL-10 promotes the

A

Treg pathway

47
Q

If there are no APC cytokines present, our Th default path is

A

Th2

48
Q

Suppresses Th1 and Th2 devo

A

TGF-B to stop inflammation

49
Q

inhibits IL-12 production and reduces expression of costims and class II MHC

A

IL-10

50
Q

tarkets NK cells and T cells to increase INF-gmma produciton, increase cytotoxic activity and Th1 differentiation

A

IL-12

51
Q

provides autocrine signal to promote more Th1 gene expression and upregulate it’s own expression

A

IFN-gmma

52
Q

these two provide autocrine signal to prmore more Treg devo

A

TGF-B and IL-10

53
Q

these promote skewing towards Th2 cells

A

IL-4 and IL-5

54
Q

INF-ggm inhibits expression of

A

IL-4… and vise versa

55
Q

this causes a class switch to IgA and prmotes eosinophilia

A

IL-5 released from Th2 cells

56
Q

This causes macrophage activation, class swithc to IgG2a, suppresses Th2 devo

A

INF-gamma

57
Q

Causes a class switch IgG1, and IgE, suppresses Th1

A

IL-4 from Th2 cells

58
Q

too much of this Th will cause autoimmunity and suspetibility to bacterial infection

A

Th17

59
Q

Although TFGB is usually anti-infl, when combinded with IL-6 and IL-23… it promotes this subset

A

Th17

60
Q

IL-17 effect on epithelial cells

A

anti-microbial peptides and increases barrier function

61
Q

IL-17 effect on leukocytes, tissues cells

A

increaes neutorlphil response

62
Q

Th1 is a master regulator of

A

T-bet transcription factor

63
Q

Th2 is master regulator of this subset

A

GATA-3 transcription factor

64
Q

TGF B alone or wth IL-10 promote _____

which is master regulator of _____-

A

T reg

Foxp3

65
Q

TGFB with IL6 and IL23 prmote _____

which is master regulator of ______

A

Th17

RORyT

66
Q

what drives the expression of genes necessary for each lineages function

A

master regulators

67
Q

What is our only FDA approved adju

A

alum

68
Q

what does ALUM do

A

promotes APC IL-4 expression to upregute Th2 devo thus increase antiB production

69
Q

B cells process and present Ag to

A

Th cells

70
Q

AntiG induced clustering of memrane Ig receptors triggers signals that are…

A

transduced by receptor-associated signal molecules

—we get tryosine phosphorylation events

71
Q

What enhances the signaling pathway of B cells once they are activated

A

binding of complement: C3d

72
Q

C3D on microbe will bind to what on B cell and whats teh results

A

binds to CR2 and increases signaling pathway

73
Q

How do T cells help B cells mediate interaction and cytokines?

A

via CD40:CD40L interation

74
Q

Once a B cell presents and antiG to T helper, what does T helper do

A

gets activated (MHC:TCR) and will express CD40ligand and secreate cytokines to the B cell

75
Q

B cell activated and releases IgM causes

A

complement activation

76
Q

Thelp releaseing IFN-y (Th1) causes B cell to isotype switch to

A

IgG subclasses….IgG1 and 3

77
Q

IgG’s are good at

A

Fc-receptor dependent phagocyte reponses; compleent activation, neonatal immunity

78
Q

Ig responsible for: Fc-receptor dependent phagocyte reponses; compleent activation, neonatal immunity

A

IgG via

via IFN-y from Th1

79
Q

complementn activation by which Ig?

A

IgM

80
Q

IL-4 released from Th2 causes B cell isotype switch to:

A

IgE

81
Q

IgE responsible for

A

immunity against helminths

mast cell degranulation

82
Q

immunity against helminths

mast cell degranulation

A

IgE

83
Q

TGF-B, cytokines and BAFF cause release of

A

IgA

84
Q

responsible for mucosal immunity and transport of this Ig through epithelia

A

IgA

85
Q

IgG binds to what receptors on macrophages to cause opsonization

A

FcyRI

86
Q

What do Fc receptor signals do?

A

activate phogocytosis and killing of ingested microbe

87
Q

Opsonization is done by what Ig and receptora

A

IgG to FcyRI

88
Q

NK celsl express

A

FcyRIIIA (CD16) for IgG

89
Q

why do NK cells expres FcRIIIA?

A

because gets coated with IgG and that will turn on antibody dependent cellular cytotoxicity (ADCC)

90
Q

What regulates granulocyte degredation?

A

Fc-e-R1 being bound by IgE

91
Q

Granclocyte activtion depends on what part of IgE

A

Fab part binds to the Ag whiles it’s Fc portion binds to the Fc-e-R2 receptor on granulocyte

92
Q

This response is cell contact dependent or independent

A

both
free floating allergens or Ag bound to surface of helmith that the Fab part of the IgE binds to then it’s Fc portion wil l bind to granulocyte

93
Q

Bindng of complement proteins to Fc regions of antiB on microbial cell surface is:

A

FcR-independent

94
Q

Antibody directed phagocytosis depends on:

A

Fc-gamma-R1 recognitoin of IgG

95
Q

Antibody directed cyytotoxicity or ADCC depends on

A

Fc-g-RIIIA-reconition of IgG

96
Q

What two cytokines are associated with NK cell lysis

A

IL-15 and IL-18

97
Q

What cytokine are associated with CD8T cell cytotoxicity

A

INF-alpha, INF-B… will increase MHC I expression and activate NK cells

98
Q

What cytokines are associated with activating macrophages?

A

INF-gamma coming from NK cells and T cells activates macrophage to phagocytize and destroy

Immunology (12 decks)

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