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Immunology (By: Ben + Dustin) > Molecules + What They Do (Ben) > Flashcards

Molecules + What They Do (Ben) Flashcards

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)
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2
Q

IL-13

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

FcƐRI

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

Mast Cell Lipid Mediators

A
  • PGD2, E2, F2α - incr. SM contraction / permeability
  • LTC4, D4, E4 - incr. SM contraction / permeability
  • LTB4 - neutrophil chemoattractant
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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)
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6
Q

Mast Cell Enzymatic Granule Contents

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

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8
Q

AIRE

A
  • transcription factor in thymic medullary epithelial cells
  • controls “promiscuous” gene expression of various antigens for process of negative selection
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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
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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)
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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)
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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)
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13
Q

CD56

A
  • NK and NKT cell surface marker
  • (plays role in cell adhesion)
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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
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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)
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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)
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17
Q

MASP

A
  • MBL-associated Serine Proteases
  • involved in MBL pathway of complement activation
  • cleave C2/C4 to form C3 convertase “C4b2a”
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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)
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19
Q

MHC III

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

C5 convertase

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

MAC

A
  • membrane attack complex
  • formed when C5b binds C6/7/8 and 10-19 molecules of C9 to form a pore
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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)
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23
Q

DAF

A
  • Decay Accelerating Factor
  • accelerates decay of C4b2a / C3bBb
  • acts as complement inhibitor
  • (lack on RBCs can -> paroxysmal nocturnal Hgb-uria)
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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)
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25
**CD59**
* AKA _MAC-inhibitory protein_ * inhibits C9 from polymerizing with C5b678 to form pore * lack can -\> **paroxysmal noctural Hgb-uria**
26
negative acute phase proteins
**transferrin**, **albumin**, **fibronectin**
27
**IL-6**
* 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
**TNF-alpha**
* 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
**IL-1**
* acute phase cytokine * secreted by _activated macrophages_, neutrophils + epithelium * vasculitis; fever induction (via hypothalamus) * induces hepatic APP production * (synergistic with TNF-alpha)
30
Hepatically-produced Acute Phase Proteins (9 items ... sorry)
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
**TAP1 / TAP2**
* TAP = **_T_**ransporter assoc. with **_A_**ntigen **_P_**rocessing * both help transport proteasome cleaved cytosolic peptides into rER to be bound to nascent **MHC-I** molecules * are ABC transporters (use ATP)
32
**CLIP**
* **_Cl_**ass-II-associated **_I_**nvariant **_C_**hain **_P_**eptide * 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
**Invariant Chain (li)**
* 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
**HLA-DM**
* binds to nascent **MHC-II** within lysosomes * removes CLIP and allow MHC-II to bind antigen peptides
35
**H-Y antigen**
* 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
**FasL**
* 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
CD28
* 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
**Foxp3**
* transcription factor expressed by Treg cells * important in normal gestational immunosuppression
39
**CCL19 / CCL21**
* 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
**CD34**
* **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
**LFA-1**
* an **integrin** on T cells * binds **ICAM-1** on endothelium during adhesion phase of extravasation * (LFA = leukocyte function-associated antigen)
42
**ICAM-1**
* AKA **CD56** * binds **LFA-1** on T cells during adhesion phase of extravasation * (ICAM = intercellular adhesion molecule)
43
**IL-2**
* T cell proliferation * "self renewal" of memory CD8+ cells after immunization * (NK / B cell activation + proliferation)
44
**HLA-B53** (probably less important, very specific + was in a seminar)
* MHC-I variant which conveys protection against _malaria_ * presents 9 AA peptides with _proline_ in position 2
45
**CD20**
* B cell surface marker
46
**CTLA-4**
* 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
B7
* 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
Cytokines involved in class switch to IgA
* **TGF-B** * IL-5 * IL-2
49
Cytokines involved in class switch to IgM
* IL-5 * IL-4 * IL-2
50
Cytokines involved in class switch to IgG
* IL-4 * IL-6 * IL-2 * **IFN-y**
51
Cytokines involved in class switch to IgE
* **IL-4** * **IL-13**
52
CD40
* 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
what two cytokines are secreted by _inflammasomes_?
**IL-1beta** **IL-18**
54
IL-12
* stimulates **Th0 --\> Th1 differentiation** * stimulates **IFNy and TNFalpha secretion** from T and NK cells * secreted by _dendritic cells_, macrophages, neutrophils
55
**PD-1 and PD-L1**
* 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
**CD1d**
* non-polymorphic MHC-I-like molecule * presents **glycolipid** molecules which are recognized by iNKT cells' invariant TCRs
57
IL-10
* anti-inflammatory cytokine produced by **Treg** and **Breg** cells * suppresses CD4+ cells * also produced by monocytes
58
**IL-7** (this one may be less important, but showed up in a figure on a slide)
maintains survival of resting naive T cells (CD4+/CD8+ cells not yet stimulated)
59
Cytokines which also stimulate adrenal corticosteroid production. Other than immune cells, where are they synthesized?
**IL-1** and **IL-6** made in **neurons**, **glia**, **pituitary** and **adrenal** **glands**
60
**H1R**
* histamine R on endothelium * HA binding increases permeability * (is other places too, this was all she said in seminar)
61
**H2R**
* histamine R on vascular SM + gastric parietal cells * causes vasoconstriction + HCl release
62
**H4R**
* histamine R on eosinophils * can recruit eosinophils to site of allergen
63
**T-bet**
* transcription factor promoting Th0 -\> Th1 differentiation
64
GATA3
* transcription factor promoting Th0 -\> Th2 differentiation
65
ROR-gamma-T | (RORyT)
* transcription factor promoting Th0 -\> Th17 differentiation
66
FGF-7 and IGF-1
* released by gamma-delta T cells to repair cells
67
**artemis endonuclease**
* 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
**TDT**
* _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
**AID** and **UNG**
* AID = activation induced cytidine deaminase * UNG = uracil-N-glycosylase * both are _somatic hypermutation_ enzymes
70
IL-2Ry
* 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
**IL-21**
* secreted by **follicular Th cells** to help B cells class switch and differentiate into plasma cells

Immunology (By: Ben + Dustin) (12 decks)

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