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Immunology > Cytokines, receptors and signaling > Flashcards

Cytokines, receptors and signaling Flashcards

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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
IL-8 made by
macrophages, endothelial cells, ep cells
26
Chemokines are good at
cauusing leukocytes to hhave increased integrin affinity, chemotaxis or activation of stuff
27
How are chemokines classified
based on number and location of N-terminal cysteine residues
28
CC, CXC, C and CX3C are secreated by ______ to promote migration of ______ to infectedsites
macrophates (or other epithelial/endothelial cells) | PMNS to site of infecion
29
Chemokines are cell contact dependend/independent
INDEPENDENT
30
Chemokines promote four stages of PMN extravasation
1. rolling 2. integrine activation by chemokines 3. stable adhesion 4. migration through endothelium
31
T cell activation requires contact ind/dependend
DEPENDENT
32
T cell activation is mediated by VDJ, VJ or both
both, needs both alpha and betta chain to function as a receptor
33
MHC, CD28, CD80 and CD86 are all exaples of
germline genes the T cell needs to get activated
34
CD28 on T cell binds to
B7 on APC
35
T cell expression of CTLA-4 results int
negatively regulating activation and competes with B7 to provide a 'stop' signal by binding to CD28
36
CTLA-4 are ____inflamatory and are contact dependent/indepentdent
ANTI inflammator | DEPENDENT
37
negatively regulating activation and competes with B7 to provide a 'stop' signal by binding to CD28
CTLA-4
38
Once TCR binds it will upregulate expression of:
CD40L expression (for B cell Ig class switching) IL2 and IL12 receptor DNA synthesis of NFAT and NFkB
39
Why does TCR upregulate CD40L once activated
key for B cell Ig class switching
40
cytokine that provides autocrine cell-contact INDEPENDENT, pro-proliferative feeback to Th cell producing it
IL-2
41
Why does TCell upregulate IL2-R once activead
because it will also release IL-2 once activated and IL-2--IL-R will cause pro-proliferaction.... autofeedback
42
This is directed by several cell-contact IND. signals produced by both APCs and Th cells themselves
Th cell differenctiation
43
APC--> IL-12 to promote Th1 expression of
IFN-gmma
44
IL-12 and IFN-gmma cause Th-->
Th1
45
TGFB makes by lots of cell types and cauaes induction to Th-->
Tregs (Th17)
46
IL-10 promotes the
Treg pathway
47
If there are no APC cytokines present, our Th default path is
Th2
48
Suppresses Th1 and Th2 devo
TGF-B to stop inflammation
49
inhibits IL-12 production and reduces expression of costims and class II MHC
IL-10
50
tarkets NK cells and T cells to increase INF-gmma produciton, increase cytotoxic activity and Th1 differentiation
IL-12
51
provides autocrine signal to promote more Th1 gene expression and upregulate it's own expression
IFN-gmma
52
these two provide autocrine signal to prmore more Treg devo
TGF-B and IL-10
53
these promote skewing towards Th2 cells
IL-4 and IL-5
54
INF-ggm inhibits expression of
IL-4... and vise versa
55
this causes a class switch to IgA and prmotes eosinophilia
IL-5 released from Th2 cells
56
This causes macrophage activation, class swithc to IgG2a, suppresses Th2 devo
INF-gamma
57
Causes a class switch IgG1, and IgE, suppresses Th1
IL-4 from Th2 cells
58
too much of this Th will cause autoimmunity and suspetibility to bacterial infection
Th17
59
Although TFGB is usually anti-infl, when combinded with IL-6 and IL-23... it promotes this subset
Th17
60
IL-17 effect on epithelial cells
anti-microbial peptides and increases barrier function
61
IL-17 effect on leukocytes, tissues cells
increaes neutorlphil response
62
Th1 is a master regulator of
T-bet transcription factor
63
Th2 is master regulator of this subset
GATA-3 transcription factor
64
TGF B alone or wth IL-10 promote _____ | which is master regulator of _____-
T reg | Foxp3
65
TGFB with IL6 and IL23 prmote _____ | which is master regulator of ______
Th17 | RORyT
66
what drives the expression of genes necessary for each lineages function
master regulators
67
What is our only FDA approved adju
alum
68
what does ALUM do
promotes APC IL-4 expression to upregute Th2 devo thus increase antiB production
69
B cells process and present Ag to
Th cells
70
AntiG induced clustering of memrane Ig receptors triggers signals that are...
transduced by receptor-associated signal molecules | ---we get tryosine phosphorylation events
71
What enhances the signaling pathway of B cells once they are activated
binding of complement: C3d
72
C3D on microbe will bind to what on B cell and whats teh results
binds to CR2 and increases signaling pathway
73
How do T cells help B cells mediate interaction and cytokines?
via CD40:CD40L interation
74
Once a B cell presents and antiG to T helper, what does T helper do
gets activated (MHC:TCR) and will express CD40ligand and secreate cytokines to the B cell
75
B cell activated and releases IgM causes
complement activation
76
Thelp releaseing IFN-y (Th1) causes B cell to isotype switch to
IgG subclasses....IgG1 and 3
77
IgG's are good at
Fc-receptor dependent phagocyte reponses; compleent activation, neonatal immunity
78
Ig responsible for: Fc-receptor dependent phagocyte reponses; compleent activation, neonatal immunity
IgG via | via IFN-y from Th1
79
complementn activation by which Ig?
IgM
80
IL-4 released from Th2 causes B cell isotype switch to:
IgE
81
IgE responsible for
immunity against helminths | mast cell degranulation
82
immunity against helminths | mast cell degranulation
IgE
83
TGF-B, cytokines and BAFF cause release of
IgA
84
responsible for mucosal immunity and transport of this Ig through epithelia
IgA
85
IgG binds to what receptors on macrophages to cause opsonization
FcyRI
86
What do Fc receptor signals do?
activate phogocytosis and killing of ingested microbe
87
Opsonization is done by what Ig and receptora
IgG to FcyRI
88
NK celsl express
FcyRIIIA (CD16) for IgG
89
why do NK cells expres FcRIIIA?
because gets coated with IgG and that will turn on antibody dependent cellular cytotoxicity (ADCC)
90
What regulates granulocyte degredation?
Fc-e-R1 being bound by IgE
91
Granclocyte activtion depends on what part of IgE
Fab part binds to the Ag whiles it's Fc portion binds to the Fc-e-R2 receptor on granulocyte
92
This response is cell contact dependent or independent
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
Bindng of complement proteins to Fc regions of antiB on microbial cell surface is:
FcR-independent
94
Antibody directed phagocytosis depends on:
Fc-gamma-R1 recognitoin of IgG
95
Antibody directed cyytotoxicity or ADCC depends on
Fc-g-RIIIA-reconition of IgG
96
What two cytokines are associated with NK cell lysis
IL-15 and IL-18
97
What cytokine are associated with CD8T cell cytotoxicity
INF-alpha, INF-B... will increase MHC I expression and activate NK cells
98
What cytokines are associated with activating macrophages?
INF-gamma coming from NK cells and T cells activates macrophage to phagocytize and destroy

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