Chemokines, Cytokines, Ect

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IL8

Back 1

secreted by Mac's, DC's and Mast cells upon PRR stimulation, induces LFA 1 and MAC 1 expression on neutrophils, also induces a low to high affinity interaction

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LFA 1

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intigrin present on neutrophils, induced by IL 8 production, binds with ICAM 1 present on endothelial cell surfaces

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P and E selectin

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endothelial adhesion molecules induced by the secretion of cytokines (TNF-α, IL-1) by Mast, Mac and DCs upon PRR stimulation

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MAC 1

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intigrin present on neutrophils, induced by IL 8 production, binds with ICAM 1 present on endothelial cell surfaces

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IL-6

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produced by macrophages induces production of acute phase proteins by the liver

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histamine

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eleased by mast cells and basophils, mast cells occupy an area in the periphery surrounding the vasculature, histamine is released and binds H2 receptors in the smooth muscle surrounding the veins and causes vasodilation.

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Lactoferrin

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produced by myeloid cells, especially neutrophils and secretory epithelial cells, binds free Fe++.

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defensins and cathelicidins

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charged proteins bind to the negatively charged bacterial surface and form pores due to their amphipathic nature

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CR1

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receptor found on the surface of macrophages, binds to C3b

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bradykinin

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from HMW kininogen (activated by kallikrein, factor XIIa and MASP1) this causes vasodilation and increased vascular permeability

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MBL

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binds to carbohydrates on the bacterial surface, MBL has associated serine proteases (MASP1 and 2) that activate C4 and C2 which together activates C3 and fixes C3b on the microbial surface

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membrane attack complex (MAC)

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C3b activation of C5 promoting its formation, formes holes in the bacterial cell membrane

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TNF-α, IL-1, and IL-6, in liver

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Secreted by macs and DC's, production of acute phase proteins (C-reactive protein, MBL, Fe binding proteins, clotting factors), causing activation of complement and opsonization

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TNF-α, IL-1, and IL-6, in BM

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Secreted by macs and DC's, neutrophil mobilization (TNF-α, IL-1, and IL-6), recruited to the site of infection by IL-8

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TNF-α, IL-1, and IL-6, in hypothalamus

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Secreted by macs and DC's, increased body temperature

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TNF-α, in DC's

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Secreted by macs and DC's, migration to lymph nodes and maturation

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primary (azurophil) granules

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antimicrobial proteins and myeloperoxidase (MPO), contains defensins

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secondary (specific) granules

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lactoferrin, NADPH oxidase

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CCL2 (monocyte chemoattractant protein 1)

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secreted by monocytes, macs and DC’s; recruits monocytes from the blood and bone marrow, second wave following PMN cells, dominant 1-2 days post infection, activated upon exposure to IFN-gamma, assist in the removal of PMN cells

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B7-1 (CD80), B7-2 (CD86)

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DC costimulatory molecules

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IFN-gamma, TNF

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Cytokines secreted by NK cells

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ITIMs

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(immunoreceptor tyrosine-based inhibition motif) binding to MHC 1 induces signal transduction and inhibition of cell killing

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ITAMs

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found on activating receptors (immunoreceptor tyrosine-based inhibition motif)

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cytotoxic granules

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containing perforin (hole puncher) and granzyme (cleaves substrates and activates apoptosis)

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FCeRI

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(IgE Fc receptor) found on mast cells

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eotaxin

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recruitment of eosinophils

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IL-5

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induces production of eosinophils in the BM

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IL-4 and IL-13, histamine

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secreted by basophils, drive TH2 response (humoral)

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NOTCH 1

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signal from thymic stroma, instructs CLP to enter T cell lineage rather than B cell lineage, also involved in the γδ vs the αβ decision

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pTα

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surrogate α chain, expressed with β, expression
on the surface with CD3 causes proliferation, arrest of further β chain
rearrangement and expression of CD4 and CD8.

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RAG

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recombinase activating gene 1 and 2: SKID mutation here, no B and T cells, recognizes specific target sequences that flank VDJ genes, cleaves hairpin and adds 'P' nucleotides

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DNA-PK

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DNA recombination and repair, defects here can also cause SKID (found in arabians with SKID)

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TdT

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Terminal deoxynucleotidyl transferase, N nucleotide addition between DNA pairs

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μ

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codes for IgM constant

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receptors expressed by CD8 T cells

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CD28, TCR, CD8

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calnexin

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Binds to MHC 1 α in the ER until β2 microglobin binds

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Calreticulin

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along with Erp58 act as chaperonins to deliver MHC 1 to tapacin

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tapacin

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provides an interaction between TAP and MHC1

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ICP47, US6

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CP47 (HSV), US6 (cytomegalovirus): prevent peptide movement through TAP

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E19

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(adenovirus): competes with tapasin and inhibits peptide loading

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US11

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(CMV): mediates retrograde translocation, MHC back into the cytoplasm to be degraded by the proteasome

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IL 2

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necessary for the proliferation of CD8 and CD4 T cells

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IFN γ, LFA 1

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upregulated in effector CD8 T cells

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Granzyme

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delivered into the cytoplasm and targets BID and procaspase 3, truncated BID disrupts the mitochondrial outer membrane and activated caspase 3 cleaves ICAD, releasing caspase activated DNase, Release of cytochrome c from the mitochondria into the cytosol activates apoptosis, CAD induces DNA fragmentation

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B7

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costimulatory molecule found on APCs, interacts with CD28

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CCR6

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expressed by immature DCs (ligand for MIP3 alpha (macrophage inflammatory protein), this is expressed by endothelial cells in response to LPS, IFN gamma and TNF)

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CCR7

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expressed by mature (activated) DCs, (ligand for MIP 3 beta)
expressed abundantly in the thymus and LN, brings activated DC’s and
activated B cells back to the LN, thought to be a receptor for bringing
memory T cells back to the LN

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Invariant chain

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binds with MHCII, blocks binding with peptides and misfolded peptides (no self binding)

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CLIP

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fragment of II cleaved in acidic endosome, bound to the MHC II binding groove

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HLA-DM

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binds to MHC II, releases CLIP, allowing other peptides to bind, MHC II then travels to the cell surface

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TCR complex

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TCR (βαζ) plus CD3 εδ-TCR- γε

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CD3

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εδ - αβTCR - γε: εδ and γε have ITAMS, there are also t zeta (ζ) chains beneath the αβTCR, that contain cytoplasmic ITAMS, αβTCR has a very small intracellular portion

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TNF α, IFN γ, and IL-12

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produced upon activation in APC's

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IL 2 receptor

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JAK/STAT pathway, JAKs cross phosphorylate, STATS bind and are also phosphorylated and activated, these then dimerise and translocate to the nucleus, act as TF's

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CTLA 4

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inhibitory molecule, out competes with CD28 for binding to B7, and when bound delivers
inhibitory signals to the activated T cell (downregulation of IL 2
receptor and IL 2) cells stop proliferating

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IL-7 and IL 15

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in conjunction with weak contact with self peptides is a survival signal for nieve T cells

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IL 12, IFN γ

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TH1 induction

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IL 4

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TH2 induction

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TGF β, IL 6

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TH17 induction

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IL-2, IFN γ

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TH 1 response, activating phagocytic cells

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IL 4, IL 5, IL 13

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TH 2 response, activating plasma cells

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IL 6 and IL 17

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TH 17 response, activating neutrophils

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IL 4

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TH 2, Stimulate naive B cells (IL 4), release after encountering B cell displaying peptide MHC II complex and CD40

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IL 13

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TH 2, Epithelial cell repair (IL 13) damage from worms

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IL 5

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TH 2 Recruit and activate eosinophils

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IL4

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Stimulate B cell to switch to producing IgE (IL 4) which promotes mast cell degranulation, Stimulation of neutralizing antibodies (IL 4) to viruses and toxins

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IL 17

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induces mobilization of neutrophils from bone marrow and recruitment to site of infection

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J chain

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Plasma cells that make IgA or IgM also secrete J chain: J chain joins Ig’s together, IgA forms pentamers, IgM forms dimers

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IgG

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most abundant: found in blood and tissues, can cross the vessels easily and hemochorial placentas.

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IgM

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large, remains primarily in the blood due to its size, pentamers bound by J chain

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IgA

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dimeric form, bound by J chain, found in the mucosa, and in mucosal secretions (saliva, tears, milk), monomeric form is found in the LN, spleen and blood.

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IgE

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surface of mast cells, basophils, mucosal eosinophils and in low concentrations in the serum, increased during allergies and nematode infections

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IgD

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mainly functions as BCR (function unknown)

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poly Ig receptor

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mediates IgA transepithelial transport transcytosis

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Fc-alpha-RI

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Promotes opsonization, binds to the Fc portion of IgA, found on phagocytes

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Fc gamma-RI

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Promotes opsonization, binds to the Fc portion of IgG, found on phagocytes

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Fc epsilon

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on mast cells, could be different antibodies, cross linking of receptors on mast cells causes granule release (histamines, leukotrienes) change permeability of vasculature.

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Fc gamma RIII

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expressed on certain NK cells, binding to Fc portion of IgG1 or 3 results in cell destruction via granule release

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C1q

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binds to either one IgM (pentamer) bound to antigen or to a few IgG molecules bound to antigen, C1q eventually results in C3 convertase activation which causes: 1. cleavage and release of C3a (mediators of inflammation, phagocyte recruitment) and 2. C3b formation which can either bind to CR1 or cause the formation of the MAC (C5 to C5a and C5b)

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C3b

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bound by RBC’s, they deliver pathogen to macrophages in the liver and spleen who bind via Fc receptors.

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α4β7

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Activated B cells home to the lamina propria via integrin α4β7 (keeps the B cell in the L propria)

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MAdCAM1

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expressed by intestinal endothelium, binds to L selectin and α4β7 on lymphocytes

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E cadherin

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intestinal epithelium expresses E cadherin, binds α4β7

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CCL25

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chemokine recruits activated lymphocytes to the lamina propria via CCR9

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NOD like receptor

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etects viral, bacterial, and non-infectious particles, induces production of IL-I, NOD mutations implicated in Crohn’s disease

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RIG-I like receptor

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RIG-I recognises 5’ triphosphate, MDA5 recognises dsRNA, induces production of IFN

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iNOS

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constitutively produces NO once arginine is produced, (nNOS and eNOS are regulated), L-arginine and molecular oxygen are the substrates and NO and citrulline are the products, NO can combine with superoxide to produce peroxynitrite which is very reactive and very damaging