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Flashcards in Molecules + What They Do (Ben) Deck (71)
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1
Q

IL-4

A
  • stimulates Th0 –> Th2 differentiation
  • is also released by Th2 cell
  • stimulates B cell isotype switch to IgE
  • antagonistic to IFN-y production (+ other Th1 cytokines)
  • (upregulates MHC-II)
  • (promotes macrophage –> M2 cell differentiation)
2
Q

IL-13

A
  • induces IgE secretion from B cells
  • (induces MMPs which are anti-inflamm. in airways)
3
Q

FcƐRI

A
  • high affinity IgE receptor (binds heavy chain Fc)
  • important on mast cells/basophils/eosinophils
  • essential in type I hypersensitivity
4
Q

Mast Cell Lipid Mediators

A
  • PGD2, E2, F2α - incr. SM contraction / permeability
  • LTC4, D4, E4 - incr. SM contraction / permeability
  • LTB4 - neutrophil chemoattractant
5
Q

IL-5

A
  • activates eosinophils in late phase type I HS reaction
  • secreted by Th2 + mast cells
  • (stimulates B cell growth / incr. Ig secretions)
6
Q

Mast Cell Enzymatic Granule Contents

A
  • carboxypeptidase
  • chymase
  • tryptase
  • (there are others, these were from lecture)
7
Q

Rheumatoid Factor

A

an IgM against your own IgG’s Fc regions

(complex settles in joints –> arthritis)

(other isotypes exist; IgM is most common)

8
Q

AIRE

A
  • transcription factor in thymic medullary epithelial cells
  • controls “promiscuous” gene expression of various antigens for process of negative selection
9
Q

CD3

A
  • T cell marker in all T cell types (starting w/ pro-thymocyte)
  • functions as TCR co-receptor
  • its ITAMs are essential for TCR signaling
10
Q

CD4

A
  • T helper cell surface glycoprotein
  • functions as TCR co-receptor in APC interactions
  • recruits Tyr kinase Lck to P-ate CD3 ITAMs for signaling
  • (sounds like too much but I had a midterm MCQ about this)
11
Q

CD25

A
  • Treg cell marker
  • (is one subunit of a high affinity IL-12 receptor)
  • (also found in T memory cells and others)
12
Q

CD8

A
  • cytotoxic T cell surface marker
  • acts at TCR co-receptor, binding MHC-I
  • recruits Tyr kinase Lck to P-ate CD3 ITAMs
  • (same as CD4 function, but in cytotoxic cells, had MCQ on this)
13
Q

CD56

A
  • NK and NKT cell surface marker
  • (plays role in cell adhesion)
14
Q

CD19

A
  • B cell surface marker
  • present in early B cell dev. stages, lost in plasma cells
  • is a BCR co-receptor
  • is intracellularly P-ated upon antigen binding, leading to recruitment of further kinases
15
Q

CD5

A
  • B1 cell surface marker
  • (lectures mentioned it as being on B1 … wiki says there is more on T cells… may not be important anyways)
16
Q

Classical C3 convertase

A
  • AKA C4b2a
  • cleaves C3 to C3a and C3b
  • (results from C1q binding C1r -> C1r cleaving C1s -> C1s cleaving both C4 + C2 and their respective b and a fragments combining)
17
Q

MASP

A
  • MBL-associated Serine Proteases
  • involved in MBL pathway of complement activation
  • cleave C2/C4 to form C3 convertase “C4b2a”
18
Q

alternative C3 convertase

A
  • AKA C3bBb
  • (formed from spontanous C3 cleavage -> C3b binds microbe + factor B -> factor D cleaves B and Ba fragment diffuses away leaving C3bBb)
19
Q

MHC III

A
  • region of chromosome 6
  • contains genes for C3b convertases (C2, C4, factor B) and TNFalpha
20
Q

C5 convertase

A
  • formed when either C3 convertase binds more C3b
  • can be C4b2a3b or C3bBb3b form
  • cleaves C5 -> C5a + C5b
21
Q

MAC

A
  • membrane attack complex
  • formed when C5b binds C6/7/8 and 10-19 molecules of C9 to form a pore
22
Q

C1 inhibitor

(deficiency = what disease?)

A
  • binds C1r/C1s/MASPs to block C2/C4 cleavage
  • thus inhibits C3 convertase production
  • deficiency = hereditary angioedema (incr. bradykinin + complement auto-activation)
23
Q

DAF

A
  • Decay Accelerating Factor
  • accelerates decay of C4b2a / C3bBb
  • acts as complement inhibitor
  • (lack on RBCs can -> paroxysmal nocturnal Hgb-uria)
24
Q

Complement Factor I

A
  • cleaves/inactivates C3b/C4b
  • substrate must first bind CR1, MCP or factor H as co-factor before Factor I can work
  • (microbes don’t have these co-factors -> complement is not inhibited from acting on them)
25
Q

CD59

A
  • AKA MAC-inhibitory protein
  • inhibits C9 from polymerizing with C5b678 to form pore
  • lack can -> paroxysmal noctural Hgb-uria
26
Q

negative acute phase proteins

A

transferrin, albumin, fibronectin

27
Q

IL-6

A
  • acute phase cytokine
  • secreted by Th2 cells and macrophages
  • induces hepatic production of other acute phase proteins
  • stimulates cortisol release (at all levels of HPA axis)
  • stimulates B cell -> plasma cell -> Ig secretion
  • (inhibits other APPs TNF-alpha and IL-1)
28
Q

TNF-alpha

A
  • acute phase cytokine
  • produced mostly by activated macrophages, also Th cells, NK cells, granulocytes
  • stimulates hepatic acute phase protein production
  • (neutrophil activation, vasculitis, cachexia, apoptosis induction)
  • (many more effects, will add later if important ones come up)
29
Q

IL-1

A
  • acute phase cytokine
  • secreted by activated macrophages, neutrophils + epithelium
  • vasculitis; fever induction (via hypothalamus)
  • induces hepatic APP production
  • (synergistic with TNF-alpha)
30
Q

Hepatically-produced Acute Phase Proteins

(9 items … sorry)

A
  1. Complement
  2. MBL
  3. CRP - opsonin/compl. activator, binds polysacchs.
  4. Serum Amyloid Protein
  5. Surfactants SP-A/SP-D - alveolar opsonization
  6. Fibrinogen - and other clotting proteins
  7. α2-macroglobulin - protease inhibitor
  8. α1-antitrypsin - protease inhibitor
  9. Ceruloplasmin - binds serum Cu ions
31
Q

TAP1 / TAP2

A
  • TAP = Transporter assoc. with Antigen Processing
  • both help transport proteasome cleaved cytosolic peptides into rER to be bound to nascent MHC-I molecules
  • are ABC transporters (use ATP)
32
Q

CLIP

A
  • Class-II-associated Invariant Chain Peptide
  • part of “Invariant Chain” (li) which binds peptide grooves of developing MHC-II within lysosomes to prevent binding of self-peptides
  • is released after HLA-DM binds MHC-II in presence of antigen peptide
33
Q

Invariant Chain (li)

A
  • binds nascent MHC-II peptide groove in rER
  • facilitates MHC-II export to acidic lysosome vesicle from rER
  • is cleaved by cathepsin S to leave CLIP fragment still bound to MHC-II
34
Q

HLA-DM

A
  • binds to nascent MHC-II within lysosomes
  • removes CLIP and allow MHC-II to bind antigen peptides
35
Q

H-Y antigen

A
  • a “minor histocompatibility antigen” in transplantation
  • incompatibility results in slower/milder rxn than MHC incompat.
  • Y-linked, male tissue-specific antigen -> transplants from same sex are best
36
Q

FasL

A
  • binds FasR receptor on other cells, inducing apoptosis
  • found on CD8+ Tc cell membranes
  • TM protein of TNF family
  • also called CD95 ligand!!! (FasR = CD95)
  • (can be solubilized by cleavage off membrane by MMP-7)
  • (exists in immune priveleged cells such as cornea to bind FasR on incoming T cells + kill them)
37
Q

CD28

A
  • T cell co-stimulatory membrane molecule
  • receives stimulation from B7 (CD80) on APCs during antigen presentation
  • CTLA4 can bind B7 in its place, and downregulate the T cell
38
Q

Foxp3

A
  • transcription factor expressed by Treg cells
  • important in normal gestational immunosuppression
39
Q

CCL19 / CCL21

A
  • constitutively expressed in lymph node
  • attract naive T cells and mature dendritic cells (via their CCR7 receptors) where antigen presentation will activate T cell and change its chemokine affinity to IL-8 so it can return to injured/infected tissues
40
Q

CD34

A
  • Hematopoietic progenitor marker (there’s an MCQ on this)
  • sialomucin (or mucosialin) adhesion molecule on high endothelial venule (HEV) cells
  • binds L-selectin on T cells in rolling phase to allow their extravasation
41
Q

LFA-1

A
  • an integrin on T cells
  • binds ICAM-1 on endothelium during adhesion phase of extravasation
  • (LFA = leukocyte function-associated antigen)
42
Q

ICAM-1

A
  • AKA CD56
  • binds LFA-1 on T cells during adhesion phase of extravasation
  • (ICAM = intercellular adhesion molecule)
43
Q

IL-2

A
  • T cell proliferation
  • “self renewal” of memory CD8+ cells after immunization
  • (NK / B cell activation + proliferation)
44
Q

HLA-B53

(probably less important, very specific + was in a seminar)

A
  • MHC-I variant which conveys protection against malaria
  • presents 9 AA peptides with proline in position 2
45
Q

CD20

A
  • B cell surface marker
46
Q

CTLA-4

A
  • alternate inhibitory receptor on T cells for B7 aka CD80 (normally co-stimulatory, but is inhibitory when binds CTLA-4)
  • (soluble CTLA-4 drugs bind B7 and block it from activating T cells via CD28)
  • (AKA CD152)
47
Q

B7

A
  • membrane molecule expressed by activated APCs
  • is co-stimulatory if it binds CD28 or inhibitory if it binds CTLA-4 on T cells
  • (has two forms (B7-1 + B7-2) with alternate names CD80 / CD86, respectively)
48
Q

Cytokines involved in class switch to IgA

A
  • TGF-B
  • IL-5
  • IL-2
49
Q

Cytokines involved in class switch to IgM

A
  • IL-5
  • IL-4
  • IL-2
50
Q

Cytokines involved in class switch to IgG

A
  • IL-4
  • IL-6
  • IL-2
  • IFN-y
51
Q

Cytokines involved in class switch to IgE

A
  • IL-4
  • IL-13
52
Q

CD40

A
  • found on B cells -> stimulation via CD40L from Th cells stimulates T-dependent IgA class switch in mucosa
  • also acts as co-stimulatory molecule on APCs for their activation -> increases its own expression + TNF-R expression + ROS/NO production
53
Q

what two cytokines are secreted by inflammasomes?

A

IL-1beta

IL-18

54
Q

IL-12

A
  • stimulates Th0 –> Th1 differentiation
  • stimulates IFNy and TNFalpha secretion from T and NK cells
  • secreted by dendritic cells, macrophages, neutrophils
55
Q

PD-1 and PD-L1

A
  • PD-1 is a programmed death receptor on activated T, B and myeloid cells
  • PD-L1 is its ligand expressed by APCs -> binds to T cell PD-1 as negative co-stimulation
  • PD-L1 can also bind to B7 (CD80) on APCs and decrease its co-stimulatory effects on CD28 on T cells (sorry)
  • (PD-1 = CD279 and PD-L1 = CD274)
56
Q

CD1d

A
  • non-polymorphic MHC-I-like molecule
  • presents glycolipid molecules which are recognized by iNKT cells’ invariant TCRs
57
Q

IL-10

A
  • anti-inflammatory cytokine produced by Treg and Breg cells
  • suppresses CD4+ cells
  • also produced by monocytes
58
Q

IL-7

(this one may be less important, but showed up in a figure on a slide)

A

maintains survival of resting naive T cells (CD4+/CD8+ cells not yet stimulated)

59
Q

Cytokines which also stimulate adrenal corticosteroid production.

Other than immune cells, where are they synthesized?

A

IL-1 and IL-6

made in neurons, glia, pituitary and adrenal glands

60
Q

H1R

A
  • histamine R on endothelium
  • HA binding increases permeability
  • (is other places too, this was all she said in seminar)
61
Q

H2R

A
  • histamine R on vascular SM + gastric parietal cells
  • causes vasoconstriction + HCl release
62
Q

H4R

A
  • histamine R on eosinophils
  • can recruit eosinophils to site of allergen
63
Q

T-bet

A
  • transcription factor promoting Th0 -> Th1 differentiation
64
Q

GATA3

A
  • transcription factor promoting Th0 -> Th2 differentiation
65
Q

ROR-gamma-T

(RORyT)

A
  • transcription factor promoting Th0 -> Th17 differentiation
66
Q

FGF-7 and IGF-1

A
  • released by gamma-delta T cells to repair cells
67
Q

artemis endonuclease

A
  • in VDJ recombination, adds palindromic sequences on the shorter strand of the gene cleaved by RAG recombinases (to match the bases on the longer strand)
68
Q

TDT

A
  • terminal deoxynucleotidyl transferase
  • adds 3-5 base pairs on end of VDJ segments after artemis endonuclease adds palindromic sequences
  • may result in a frame shift, and this is the mechanism for “junctional diversity” of VDJ recombination
69
Q

AID and UNG

A
  • AID = activation induced cytidine deaminase
  • UNG = uracil-N-glycosylase
  • both are somatic hypermutation enzymes
70
Q

IL-2Ry

A
  • IL-2 receptor that is mutated in SCID (severe combined immunodeficiency disorder)
  • issues with RAG recombinases in this disease lead to no lymphocyte function
71
Q

IL-21

A
  • secreted by follicular Th cells to help B cells class switch and differentiate into plasma cells