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Physiology > Interleukins and other messengers/markers > Flashcards

Interleukins and other messengers/markers Flashcards

1
Q

IL-3

A

HSC differentiation: common myeloid progenitors / with IL-7, B cells

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2
Q

GM-CSF

A

HSC differentiation: common myeloid progenitors / monocytes/macrophages

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3
Q

IL-7

A

HSC differentiation: common lymphoid progenitors / with IL-2, T cells / with IL-3, B cells

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4
Q

IL-4

A

HSC differentiation: basophils

Immune respones: strong activator of BCs and signature cytokine of Th2 response. Inhibits TMMI/Th17

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5
Q

G-CSF

A

HSC differentiation: neutrophils

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6
Q

IL-5

A

HSC differentiation: eosinophils

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7
Q

M-CSF

A

HSC differentiation: Monocytes/macrophages

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8
Q

Flt3L

A

HSC differentiation: Dendritic cells

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9
Q

IL-2

A

HSC differentiation: with IL-7, T cells
TMMI: self-sustaining signal produced by Th1’s after antigen binding + IL12/18 - critical growth cytokine
also enhances NK and B cell responses
absolutely required for survival of Tregs (cannot produce their own

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10
Q

C1

A

Initiator of classical pathway of complement activation. Composed of C1qrs. Q must bind/crosslink 2 Ab Fc regions. r has proteolytic activity on s. s cleaves C4; then C2 when part of the C4b2 complex, creating C4b2a, a C3 convertase

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11
Q

C4

A

The classical complement pathway protein cleaved by C1s to C4a/b. C4b BINDS TO THE PATHOGEN SURFACE, associates with C2 (cleaved by C1s to C4b2a) to create a C3 convertase

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12
Q

C2

A

The classical complement pathway protein that associates with membrane bound C4b and is cleaved by C1s to create the C3 convertase, C4b2a

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13
Q

MBL

A

Mannan-binding lectin. One of two initiators of the lectin pathway of complement activation (compare to C1). Binds directly, with high avidity, to mannose and fucose residues.

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14
Q

MASP-1

A

mannan binding lectin associated serine protease 1. Compare to C1r; activates MASP-2

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15
Q

MASP-2

A

mannan binding lectin associated serine protease 2. Compare to C1s; cleaves C4 and, once C4b binds the pathogen and associates with C2, creates C4b2a

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16
Q

C3

A

Complement pathway protein. C3b binds membrane and acts as a powerful opsonin (rapidly degraded unless it binds a membrane though).
Also complexes with C4b2a to create a C5 convertase. C3a is a soluble inflammatory mediator
C3 also undergoes low levels of spontaneous hydrolysis in serum, at which point it can bind Factor B and allow its cleavage by Factor D to create a C3 convertase. C3bBb3b becomes a C5 convertase

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17
Q

C5

A

Final common complement pathway protein; cleaved by C5 convertase C4b2a3b OR C3bBb3b. Generation of 5b initiates the final stage of complement activation, formation of the MAC 5a is a soluble inflammatory mediator.

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18
Q

Ficolin

A

One of two initiators of the lectin pathway of complement initiation. It recognizes acetylated oligosaccharides. It is associated with MASP-1 and 2: compare C1qrs

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19
Q

Factor B

A

Alternative complement pathway protein. Complexes with C3(H2O) and is hydrolyzed to C3(H2O)Bb to form a C3 convertase.
May also complex with membrane bound C3b, be cleaved by Factor D, then stabilized by properdin to form a membrane bound C3 convertase C3bBb.
Complexes with a second C3b to form a C5 convertase, C3bBb3b.

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20
Q

C6-9

A

Proteins that participate in forming the MAC in the final common complement pathway (C5b67 complex binds to cell via C7; C8 inserts into membrane; a whole bunch of C9 punches a hole into membrane. Gram-negative only

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21
Q

CR1

A

AKA CD35
C3b receptors found on phagocytes (esp neutrophils and macrophages) that facilitate phagocytosis of opsonized pathogens. This process is facilitated by C5a.
Also found on erythrocytes allowing for the carrying to and clearance of immune complexes by the spleen and liver.
Can also inhibit C3 convertase, C5 convertase

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22
Q

C5a

A

soluble inflammatory mediator released when C5 is cleaved by a C5 convertase. Important in recruitment of leukocytes; facilitation of phagocytosis; triggering granule release on mast cells and basophils. This last property makes it (along with 4a and 3a) an anaphylotoxin (and inflammatory mediator)

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23
Q

C4a

A

Soluble split product of C4. Capable of causing degranulation of mast cells/basophils. Anaphylotoxin and inflammatory mediator

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24
Q

C3a

A

Soluble split product of C3. Capable of causing degranulation of mast cells/basophils. Anaphylotoxin and inflammatory mediator.

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25
Q

C1INH

A

C1 Inhibitor. Regulation of complement activation. Inhibits C1 by dissociating C1r and C1s from C1q

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26
Q

DAF

A

AKA CD55
Decay-accelerating factor. Regulates complement activation by inhibiting (classical) C3 convertase

May be given clinically

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27
Q

C4Bp

A

C4 binding protein. Regulates complement activation by inhibiting (classical) C3 convertase

28
Q

MCP

A

Membrane cofactor protein. Regulates complement activation by inhibiting (classical) C3 convertase

29
Q

Factor I

A

Regulates complement activation by inhibiting C5 convertase

30
Q

Factor H

A

Regulates complement activation by inhibiting C5 convertase

31
Q

CD59

A

Regulates complement activation by preventing assembly of MAC

32
Q

Factor P

A

aka properdin. Stabilizes C3bBb complex on pathogen membrane to form C3 convertase

33
Q

CCL21

A

chemokine secreted by stromal cells and HEV’s of lymph nodes. chmokine attracts DC’s, which express a CCL21 receptor

34
Q

CCL18/19

A

chemokine secreted by DC’s to attract TC’s, BC’s to a developing lymph node

35
Q

CXL13

A

chemokine secreted by follicular DC to attract BC’s to developing germinal center

36
Q

CCR7

A

“homing receptor” (for CCL7?) directs TC’s to Peyer’s patches

37
Q

L-selectin

A

directs TC’s to Peyer’s patches

38
Q

IL-8

A

potent neutrophil chemoattractant

39
Q

sIgA

A

secretory IgA; dimeric, connected by a J chain and secretory component (remainder of pIGR from trancytosis through epithelium)

40
Q

pIGR

A

poly-Ig Receptor - binds to dimeric IgA or pentameric IgM to transcytose
found in basement membrane of mucosal epithelium. cleaved portion at exocytosis forms secretory component

41
Q

TSLP / TGF-β / PGE2

A

Triad of cytokines in the gut that inhibit dendritic cell maturation - found in presence of commensal bacteria
(cause DC’s give weak co-stimulatory signals which induce Tregs)

42
Q

IL-12

A

along with IL-18, initiating cytokine, produced by an APC, that drives a TMMI

43
Q

IL-18

A

secondary cytokine (with IL-12) produced by an APC, that drives a TMMI

44
Q

T-bet

A

the “master transcription factor” that defines a Th1 CD3/CD4 T cell

45
Q

IFN-g

A

signature cytokine of an ongoing TMMI. produced first by an activated Th1. (may also be produced by NK cells, activated CD8 or δs)
powerful chemokine, activator of macrophages and the endothelium, and upregulator of MHC presentation
potent inhibitor of Th2/17 response

46
Q

IL-1, IL-6, IL-8, TNFα

A

The TMMI “classic tetrad” of proinflammatory cytokines

47
Q

IL-21

A

very potent activator of CD8’s in the presence of IFNg

In the presence of IL-4, stimulates proliferation/ differentiation/survival of B’s

48
Q

IL-1

A

prototype inflammatory cytokine - broad effect to stress/infection
(with IL-6) can cause fever via hypothalamus; mobilize neutrophils and upregulate leukocyte production
Neuroendocrine: acts through pituitary to cause release of ACTH in response to stress

49
Q

IL-6

A

synergistic with IL-1
differs from IL-1 in that it acts in the bone marrow: stimulates BC growth and differentiation; promotes bone remodeling (involved in postmenopausal osteoporosis?)

50
Q

TNFα

A

under inflammatory conditions, activates M/M, endothelium, promontes vasodilation

51
Q

IL-1ra

A

naturally occurring antagonist of IL-1 (competes for receptors) - prevents morbidity of a runaway immune response
produced by microglia of brain to help maintain CNS immune quiescence

52
Q

KIR

A

killer cell inhibitory receptor
expressed on NKC’s, recognizes NORMAL MHC. abnormal? cytotoxicity
(if cell lacks MHC, NKC will only “notice” it if it has an NK activating receptor - good for RBC’s)

53
Q

IL-10

A

strong promoter of BC differentiation/isotype switch/proliferation
BUT ALSO very potent downregulator of TMMI; important for Tregs
Mutations in receptor associated with IBD

54
Q

TGFβ / IL-6 / IL-23

A

Triad that influences Th17 development

55
Q

MHC-II (D)

A

MHC DR locus most strongly predictive of graft survival

MHC-D, certain polymorphisms strongly correlated with atopy/allergy, autoimmunity

56
Q

CD16

A

Fc receptor necessary for antibody directed cytotoxicity (ADCC)
NK cells in the gravid uterus LACK this receptor

57
Q

Leptin

A

Adipocytokine.
Decreases appetite [upregulated in obesity though].
Pro-inflammatory: increases production of IL-1, 6 and TNF (gamma??) especially by macrophages

58
Q

Adiponectin

A

Adipocytokine. Stimulated by MAC-1
Anti-inflammatory: suppresses TNF alpha
Major antagonist to leptin

59
Q

MAC-1

A

Adipocytokine
Macrophage Inhibitory Cytokine-1 [member of TNF superfamily]
Anorexigenic (serum levels negatively correlate with body mass)
Anti-inflammatory: Major stimulator of adiponectin

60
Q

Visfatin

A

Adipocytokine strongly expressed in white adipose tissue
Pro-inflammatory
**Pro-angiogenic [therapeutic target?]

61
Q

Osteopontin

A

Macrophage derived cytokine in white adipose tissue
Pro-inflammatory
Strongly chemotactic for M/M

62
Q

Resistin

A

Macrophage derived cytokine in white adipose tissue
Pro-inflammatory (direct antagonist of adiponectin)
Promotes TNFalpha and IL-6

63
Q

CCL2

A

Monocyte chemoattractant protein 1
Secreted by adipocytes
potent chemoattractant for macrophages

64
Q

PD-1

A

Programmed death receptor

Inhibitory TC receptor ON CYTOTOXIC T’s [compare CTLA-4]. When engaged by PD-L1 or -2, the TC is killed or paralyzed

65
Q

CTLA-4

A

Inhibitory T-cell receptor, expressed by CD4/25/FoxP3 T’s. Activated by B7; prevents second signal for activation, promotes Treg status or anergy

66
Q

PD-L1/2

A

Programmed death receptor ligand 1/2
Interacts with PD-1 on TC’s causing paralysis or death
Upregulated on some tumors as a defense mechanism

Physiology (8 decks)

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