Glossary of Cytokines and Receptors

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IL-2 (IL-2 Superfamily)
Adaptive Immunity. Produced by naive T cells. IL-2 production and IL-2 receptor expression requires Ag recognition by the T cell. The IL-2 receptor is an autocrine receptor that increases T cell proliferation; also causes proliferation of NK and B cells; and potentiates apoptotic death of Ag-activated T cells in a negative feedback mechanism.
IL-7 (IL-2 Superfamily)
Adaptive Immunity. Produced by fibroblasts, bone marrow and stromal cells. IL-7 is essential for the survival and proliferation of naive B and T cells in lymphoid organs.
IL-15 (IL-2 Superfamily)
Adaptive Immunity. Similar IL-2, but produced by APCs and other non-lymphoid cells. Stimulates the proliferation of NK cells and CD8+ cells, particularly CD8+ memory cells.
IL-4 (Small family including IL-13)
Adaptive Immunity. Produced by Th2 cells and Mast Cells. IL-4 is a B-cell growth factor; Mast cell proliferator; increases production of MHC II; induces B cell isotype switch to IgE; induces Th2 differentation from Th0; inhibits IFN-γ; increases mast cell proliferation and degranulation.

IL-13 has the same effects b/c it binds to the same receptor; also causes mucus production (asthma & allergic rxns)

Both IL-4 and IL-13 are produced in allergic rxns; IL-4 inhibitor drugs can be used to treat allergies and asthma.
IL-6 (Large family including G-CSF)
Innate (XX) > Adaptive (X) Immunity

Produced by MΦs and Th2 cells; Growth factor for plasma cells (elevated in multiple myeloma); Has endocrine (and paracrine) action.

IL-6 is an endogenous pyrogen that causes fever and AFR (acute phase reactants) production in the liver.
Secreted by TH2 cells and regulatory T cells. Decreases the TH1 response (like TGF-beta) by suppressing antigen presentation. (IL-10 knockouts have IBS). If lost, autoimmunity can develop. IL-10 inhibits APCs by decreasing IL-12 secretion and B7 expression. IL-10 inhibits MΦs.
IL-12 (Small family w/IL-23)
Innate (XX) > Adaptive (X) Immunity

IL-12 induces Th1 differentiation from Th0. It is secreted by activated MΦs and activates NK cells. Vaccines have been developed to target IL-12 to increase the Th1 response.
IFN-γ (a type II IFN)
Innate & Adaptive Immunity

IFN-γ is secreted by Th1 cells and NK cells; paracrine signaling; causes activation and proliferation of MΦs to phagocytose bacteria; increases expression of MHC I and II; induces B cell isotype switching to IgG; stimulates monokine expression (e.g., IL-1); stimulates NK cells; induces T cell adhesion to endothelia; induces Th1 differentiation from Th0; important for DTH rxns (e.g., PPD test); helps from granulomas; produced when intracellular bacteria or parasites are present; anti-viral response; clinically used to treat chronic granulomatous disease (stimulates phagocytosis), drug resistant TB, and pulmonary fibrosis.
Made by at least 20 different genes (same as IFN-β). Activates the JAK/STAT pathway. STATs dimerize and translocate to the nucleus. IRF is phosphorylated and translocates to the nucleus. Gene targets are: IFN-α for positive feedback, p21, IL-15, FasL, and IL-12.
IL-1 (alpha and beta from different genes but have the same effects)
Adaptive Immunity. Family of TLRs/IL-1 Receptors. IL-1 is produced by activated MFs and other cells. Acts upon many target cells: (1)FIBROBLAST proliferation and increases fibroblast production of prostaglandin E2 and collagen; (2) SMOOTH MUSCLE CELL proliferation; (3) CHONDROCYTE proliferation, increased secretion of proteases and collagenases, response to IL-1 injection resembles rheumatoid arthritis; (4) SYNOVIOCYTE proliferation and increased secretion of proteases and collagenases;(5) OSTEOCLAST proliferation and activation for bone catabolism; (6) HEPATOCYTE activation to secrete acute phase reactants; (7) HYPOTHALAMUS by induction of prostaglandin (fever, anorexia, sleepiness, CRF production);(8) ENDOTHELIUM becomes "sticky" via production of integrin ligands.

**Also activates clotting factors. IL-1RA is an endogenous inhibitor to the IL-1 receptor.
IL-18 (TLR/IL-1R family)
Innate (XX) > Adaptive (X)

Structurally homologous to IL-1; produced by MFs in response to LPS; stimualtes production of IFN-γ by NK cells (synergizes with IL-12); an inducer of cell-mediated immunity.
IL-18 (TLR/IL-1 Receptor Family)
Innate (XX) > Adaptive (X) Immunity

Structurally homologous to IL-1; produced by MFs in response to LPS; stimulates production of IFN-γ by NK cells (synergizes with IL-12); an inducer of cell-mediated immunity.
LT-alpha (TNF Related Receptors)
Innate (X) < Adaptive (XX) Immunity

Increases expression of MHC I
Innate Immunity

Does everything IL-1 does; secreted as a homotrimer from activated MFs and binds to a trimeric receptor; causes tissue necrosis; lysis of tumors; TNF-α is a major mediator of response to Gram neg. infections; increases expression of MHC-I and MHC-II.
Expressed when T cell is activated and provides a second signal to B cells (complement does the same). When it engages with CD40, it activates the NFκB signaling pathway.
FasL is located on activated T cells. When it binds Fas, it leads to Caspase 8 activation. This type of cell death results from continued exposure to Ag.
Adaptive and Innate Immunity

Stimulates B cell isotype switch to IgA; inhibits T and B cell proliferation and antagonizes the actions of IFN-gamma; made by Th3 cells; important in wound repair.
Secreted by TH2 cells. Leads to proliferation of eosinophils. Important in asthma, allergy, and response to parasitic infections.
Secreted by DCs and MΦs. IL-8 is a chemokine secreted during the acute phase response. It attracts neutrophils (PMNs).
Secreted by TH2 cells. Stimulates the TH2 pathway. Involved in allergy and asthma.
Made predominantly by fibroblasts; produced by inefcted cells to keep other cells from becoming virally infected - used in paracrine signaling to save neighboring cells; inhibits proliferation of neighboring cells (many viruses require host cell proliferation); activates NK cells; increases expression of MHC-I; induces production of anti-viral proteins (e.g. 2,5-oligoadenylate synthetase).
Colony Stimulating Factors
These promote growth and differentiation of early hematopoietic precursors from the bone marrow. M-CSF is for monocytes, G-CSF is for granulocytes, and GM-CSF is for both. GM-CSF might be given to increase WBC count after chemotherapy.
CD3 is expressed with the TCR beta chain, and they appear together on the cell surface. CD3 is composed of five chains: gamma, delta, epsilon, and 2 zeta chains. CD3 gets phosphorylated on ITAMs on the zeta chains. Interepithalial lymphocytes (IELs), which are CD8+, express high numbers of CD3.
Expressed on T cells and monocytes/MFs. Expressed with CD8 on T cells after the TCR is fully formed. Thus, when an αβTCR on present (with CD3) on the double negative T cell, it engages signaling pathways which result in the expression of CD4 and CD8 on the cell membrane, making DP T cells.
Expressed on CTLs. Signaling and adhesion coreceptor for MHC Class I; thymic dendritic cells express CD8alpha
Expressed on leukocytes; involved in cell-cell adhesion; binds ICAM-1, -2, and -3
CR3 (also known as CD11b)
Expressed on granulocytes, monocytes, MFs, NK cells, and mast cells. Integrin that functions as a receptor for iC3b; promotes phagocytosis of microbes opsonized with iC3b; neutrophil and monocyte adhesion to endothelium and EC matrix proteins.
Binds the LPS-LBP complex with TLR4 to activate MFs to release cytokines and attract other inflammatory cells. The MF will bind CD14 prior to binding TLR4. CD14 recognies all LPS molecules. It can also recognize Gram positive bacteria.
Expressed on NK cells, MFs, mast cells and neutrophils; immune complex-induced cellular activation; Ab dependent cellular cytotoxicity; Fc receptor for IgG; involved in neutrophil activation
CD18 (β2 Integrin Subunit of LFA-1 and CR3)
Expressed on leukocytes and has all the functions of LFA-1 and CR3: involved in cell:cell adhesion; binds ICAM-1,2, and 3; functions as a receptor for iC3b; promotes phagocytosis of microbes opsonized with iC3b; neutrophil and monocyte adhesion to endothelium and EC matrix proteins.
CR2 (also known as CD21)
Present on mature B cells and follicular DCs; receptor for complement C3b which binds to microbes and promotes trapping of Ab-Ag complexes in germinal centers; triggers B cell growth; involved in EBV recognition.
IL-2 Receptor α Chain (CD25)
Present on activated T cells, as well as B cells and MΦs. Regulatory CD4+ cells express high levels; binds IL-2.
FcγRIIA and FcγRIIB (CD32)
Present on MFs, granulocytes, B cells, eosinophils, and platelets.

Fc receptor for aggregated IgG; binds C-reactive protein; important in phagocytosis; acts as an inhibitory receptor that terminates activation signals initiated by the B cell antigen receptor.
CR1 (CD35)
Present on erythrocytes. Binds to the immune complex and transports C3b and iC3b bound to IgG-antigen to the liver or the spleen. Macrophages then break the complex from the RBC and digest the complex. The erythrocyte is returned to circulation, but CR1 gets damaged with each interaction. CR1 enhances ADCC.
Present on APCs and endothelial cells; binds to CD40L on activated T cells; binding enhances expression of B7 costimulator on APCs; part of CR2-CD19-CD81 complex; plays a role in T-cell dependent APC and endothelial cell activation.
α4 integrin subunit (CD49d)
Expressed on T cells, monocytes and B cells. Involved in leukocyte adhesion to endothelium and ECM; binds to VCAM-1 and MAdCAM-1; binds fibronectin and collagens.
ICAM-1 (CD54)
Present on endothelial cells, T cells, B cells, and monocytes. Involved in cell-cell adhesion; ligand for LFA-1 and Mac-1; receptor for rhinovirus.
Present on B cells, T cells, monocytes, granulocytes, and some NK cells. It is a receptor on naive lymphocytes to bind to PNAds (e.g., GlyCAM-1, CD34, MAdCAM-1) on HEVs; leukocyte-endothelial adhesion; homing of naive T cells to peripheral lymph nodes.
Present on monocytes, MFs, and activated neutrophils. High affinity Fc receptor. Plays a role in phagocytosis and MF activation.
Present on mature B cells. Required for cell surface expression of and signal transduction by the B cell antigen recognition complex.
B7-1 (CD80)
Present on activated APCs. Costimulator for T cells increased by endotoxin and IFN-γ. B7-1 allows T cell activation upon binding with CD28 (this is the ligand for CD28 and CTLA-4)
B7-2 (CD86)
Present on activated APCs, also expressed on some monocytes and T cells. Costimulator for T cells increased by endotoxin and IFN-γ. Allows T cell activation upon binding with CD28. Ligand for CD28 and CTLA-4.
C5a Receptor (CD88)
Present on granulocytes, DCs, and mast cells. Receptor for C5a complement fragment. Has a role in complement-induced inflammation.
Fas Receptor (CD95)
TNF family member. Mediates activation-induced T cell death. Binds FasL. Repeated CD4+ activation increases Fas receptor and FasL.
VCAM-1 (CD106)
Present on endothelial cells, MFs, Follicular DCs, and marrow stromal cells. Important for adhesion. Receptor for VLA-4 integrin.
IFN-alpha/beta Receptor (CD118)
Present on many cells! Binds and mediates the effects of IFN alpha/beta.
IFN-γ Receptor (CD119)
Present on MFs, monocytes, DCs, B cells, T cells, endothelium, and epithelial cells. Binds and mediates the effects of IFN-γ.
TNF-R1 (CD120a)
Present on many cells. Binds and mediates most effects of TNF-alpha and TNF-beta.
Type I IL-1 Receptor (CD121a)
Present on mnay cells. Binds and mediates the effects of IL-1.
Common γ chain (of IL-2, IL-4, IL-7, IL-9, and IL-15 receptors), also known as CD132
Present on T cells, B cells, NK cells, monocytes, MFs, and neutrophils. Responsible for some of the signaling functions of the receptors for IL 2, 4, 7, 9, and 15.
CTLA-4 (CD152)
Present on activated CD4+ T cells. This is the inhibitory version of CD28. It binds B7-1/2. It is expressed on activated T cells; terminates the T cell response, plays a role in self-tolerance by inducing anergy in T cells as they recognize self antigen.
CD40L (CD154)
Present on activated CD4+ T cells. Activates B cells, MFs, and endothelial cells. It is the ligand for CD40.
PSGL-1 (CD162)
Present on T cells, monocytes, granulocytes and some B cells. It is a ligand for selectins, and is involved in the adhesion of leukocytes to the endothelium.
Present on activated T cells, NK cells, tumor cells, retinal cells, and endothelial cells. Broadly inducible. Binds Fas. Induces apoptosis via the Fas pathway.
CXCR4 (fusin)
Present on many blood and tissue cells. This is a receptor on naive B cells, recognizing chemokine (SDF1) made only in lymph follicles (B zone) and attracts naive B cells to the B zone; cofactor for T cell-tropic HIV entry into cells later in the course of disease.
This chemokine receptor is found on activated DCs and naive T cells, and leads them both to traffic to the T cell zone of the lymph node. CCR7 is upregulated with DC maturation so that the DCs can "see" the chemokines secreted by the lymph node T cell zone.
Found on nucleated cells. ABC stands for ATP-Binding Cassette domain on TAP 1,2 which hydrolyzes ATP for peptide transport into the ER.
Acute Phase Reactants/Proteins
Responsible for angiogenesis in rheumatoid arthritis. Stimulated by IL-1 and TNF to be released from hepatocytes. Cause systemic symptoms.
Antibody-dependent cell mediated cytotoxicity. Kill via NK, MF, or neutrophils which recognize the Fc portion of the opsonizing Ab. Antibodies also activate the classical pathway where C3b interacts with CR1 to enhance ADCC.
Added to an antigen in vaccine to get the immune response. E.g., Complete Freund's Adjuvant = mineral oil and killed mycobacteria, which activate DC through the TLR.
Attachment proteins on an adenovirus recognize receptor proteins in the host that are similar to Ig.
Involved with mutations in the variable region during somatic hypermutation. ssDNA is generated during variable region transcription and AID deaminates these segments. Repair mechanisms then cause the mutations. AID is both necessary and sufficient to cause hypermutation. Also needed for isotype switching, which occurs at the same time as somatic hypermutation.
Present on T cells post recombination of the alpha chain, which follows successful recombination of the beta chain. Cells that express the αβ-TCR are double positive (or have moved on to be single positive).
Anti-nuclear antibodies. Test for ANAs to confirm whether patients have SLE. ANAs are characteristic of SLE.
Artemis nicks the hairpin loop to form a staggered end. Once the mutations have been added to increase variability of the immune repertoire, the DNA is rejoined by DNApkc, ku70/80, XRCC4, and ligase IV.
Present on nucleated cells. This is the part of the MHC Class I molecule that binds to the alpha chain-antigen complex after they have associated in the ER. Constant. Doesn't enter the cell membrane and is not encoded in the MHC.
B1 cells
These lymphocytes elaborate IgM. They make only natural antibodies, which are low affinity.
Sees proteins, carbohydrates, nucleotides in linear or conformational form. Overexpressed in lymphomas.
Upregulated in tumor cells to prevent Fas-mediated killing by NK or CD8+ T cells.
C Reactive Protein
Helps eliminate pathogens in the acute phase response.
Calmodulin binds calcineurin to make the active calcineurin phosphatase which dephosphorylates NFAT which then enters the nucleus to activate gene expression.
Calmodulin is activated by an increase in intracellular Ca2+ due to IP3. Binds to calcineurin to create the active calcineurin phosphatase.
Inhibits C1, kallikrein, factor 12, plasmin. C1-inhibitor is missing in hereditary angioneurotic edema.
C1q is the first component in the complement pathway. It binds to Abs complexed with Ag. Must have at least 2 Abs for cross-linking and C1q activation. Is also helpful for transporting apoptotic waste for removal/clearance.
C1r and C1s
Intertwined with C1q in the classical pathway for complement activation. Inactive until C1q binds Ab, at which point C1qC1rC1s cleaves C2 and C4 to produce the C2aC4b complex = C3 Convertase.
In the classical pathway, C2 binds to C4b to form the C3 convertase.
Defends against bacteria with the complement cascade. The classical and alternative systems of complement activation converge at C3. Triggers MAC assembly or makes bacteria available for phagocytosis (opsonization). Spontaneously activated by attacking H2O which hydrolyzes its ester bond. C3b will attach to bacterial surfaces and opsonize them in both the classical and alternative pathways of complement activation. In the alternative pathway, C3b binds Factor B.
C3a, C4a, C5a
Anaphylatoxins: induce inflammation, smooth muscle contraction, increase vascular permeability, cause mast cell degranulation. Can cause anaphylaxis in large amounts. Can also induce vascular adhesion molecules.
Part of the alternative pathway of complement activation. Activates C3 and amplifies the alternative pathway. Activity is stabilized by Factor P.
Inhibitors for C3 and C4 turn C3b into iC3b. This is the inactivated form of C3b, which binds to MF complement receptors (CD3)and causes breakdown and digestion of phagocytosed products.
C3dg was once activated C3 that was cleaved into C3a and C3b. C3dg binds to CR2 on B cells and activates them.
C5 Convertase
Activates C5, which interacts with C6, C7, C8, to form a complex on the pathogen's cell membrane. When this complex binds to C9, C9 is polymerized and that MAC is formed.
Downregulated with DC maturation. These chemokine receptors are displayed on resting DCs.
This receptor is present on CD4+ T memory cells, DCs and monocytes/MFs. It is required for HIV fusion, allowing M-tropism (period during which HIV can enter MFs). It is a chemokine receptor that combines with CD4 in the membrane viral receptor complex. "R5 tropic" strains bind to CCR5. RANTES, MIP-1a and MIP1b are endogenous ligands for CCR5. These inflammatory cytokines are produced by CD4+ and CD8+ T cells in response to HIV infection, and compete with HIV for CCR5 binding. These endogenous chemokines block viral entry and keep the patient relatively asymptomatic. At this point the virus does not infect naive T cells. R5 tropic strains of the virus replicate in monocytes, where most of the viral load is. CD4+ T cell count is decreased but stable. The R5 tropic form is nearly ALWAYS the sexually transmitted form of the virus.
MHC I-like molecule encoded in the MHC locus. Binds to bacterial glycolipids.
This is expressed on the earliest form of T cell expressed in the thymus, the double negative cell. It is the first receptor expressed on a T cell during its development.
CD3-zeta chain
TCR is engaged via interaction with MHC-peptide complex, leading to phosphorylation of CD3-zeta chain, which recruits ZAP-70 (a tyroskine kinase). T cell becomes anergized if there is ↓ tk (ZAP-70) activity and ↓ Ca2+ influx, leading to reduced NFκB and JNK transcription factor translocation into the nucleus.
CD4+/CD25+ T cell
This is a regulatory T cell. It inhibits the immune response by stopping T cell proliferation. Suppresses IL-2. T regulatory cells get activated by interacting with peptide-MHC II, then secrete suppressive cytokines such as IL-10 and TGF-beta. Compete for B7 binding on the APC with the CTLA-4 expressed on their surface.
CD8+ T cell
CD8 is expressed with CD4 after the αβTCR/CD3 is placed on the cell surface (after successful α chain rearrangement). CD8+ T cells kill virally infected self cells expressing MHC I. Detect whether cells are displaying self or viral antigens on their MHC I. CD8+ T cells require CD28-B7 costimulation for activation. IL-2 and IFN-gamma also provide stimulatory/activation signals to CD8+ T cells. Upon activation, make perforin and granzymes, and express FasL to kill cells that express Fas. Secrete TNF to kill tumor cells.
CD8 Suppressor
Involved in oral tolerance. See lecture materials for more details.
Shared tumor antigen for B cells. Not expressed on plasma B cells, but it is present on all the other varieties of B cell.
CR2 (CD21)
Present on B cells. Can be bound by C3dg, which activates the B-cell to digest immune complexes. Binding of C3d recruits PI-3 kinase which increases PIP3 levels, thereby increasing cell sensitivity to signaling.
IL-2 receptor
CD28/B7-1 (CD80)
Second costimulatory signal for T cell activation, which initiates activation of naive T cells.
CD40L is expressed on T cells, CD40 on APCs. This interaction activates the DC causing it to secrete interleukins; causes somatic hypermutation of B cells; causes germinal center formation.
Inhibitory product that binds to the surface of the RBC or platelet and prevents complement from binding and destroying it in Paroxysmal Nocturnal Hemoglobinuria.
Region on Ig where the Ab contacts Ag. This is at the N-terminus.
Hypervariable region at the VJ light-chain joint and VD and DJ heavy chain joints.
Serial dilution demonimator at which there is lysis of 50% of RBCs.
What is the function of a chaperone?
These proteins on all nucleated cells help the α-chain of MHC Class I bind to Ag.
CLIP is found on APCs. It is the fragment of the invariant chain bound to MHC-I after degradation by proteases. It is released by HLA-DM, which permits peptide binding.
Combinatorial Association
Combinatorial Joining
Light Chain + Heavy Chain
There is a deficiency of CR3 in LAD. CR3 (MF complement receptor) binds to iC3b to mediate phagocytosis and breakdown of immune complexes. Recognizes beta-glucan on the cell wall of bacteria and fungi.
Present on phagocytes. There is a deficiency of CR4 in LAD.
What happens if you lack CTLA-4?
Autoimmunity! No tolerance or anergy of T cells is possible without CTLA-4. It competes with CD28 for B7 on APCs.
Required for HIV fusion, allowing T-tropism whereby HIV can only enter naive T cells. HIV strains that bind CXCR4 are "R4 trophic" and cause SDF-1 ligands to be made by stromal cells, which compete with HIV binding. This strain infects naive and activated T cells. (SDF-1 causes the migration and homing of T cells to the lymph nodes.) The HIV virus will mutate from R5 to R4 with a change in the viral envelope V3 loop, resulting in severe immune deficiency and full-blown AIDs.
Present on Naive B cells. Chemokines from lymphoid follicles bind to CXCR5 on B cells and direct their movement towards the lymph node.
Cryptic Promoter
T cells send cytokine signals to the B cells. The cryptic promoter region is upstream of the heavy chain lcous, and specifies the switch region where the heavy chain locus will be cut. Determines which isotype will be made (IgG, IgA, IgE?)
Cytochrome C
With neglect, cytochrome C is released from the mitochondria and activates caspase 9, leading ultimately to cell death.
Inhibitory product that binds to the RBC or platelet to prevent complement from binding in Paroxysmal Nocturnal Hemoglobinuria (w/CD59).
Split product of PIP2. Activates PKC which phosphorylates IkappaB (an NFkappaB inhibitor). This permits NFkappaB to enter the nucleus and activate gene transcription.
Dark Zone of the Germinal Center
B cells proliferate in the dark zone of the germinal center, and undergo somatic hypermutation. If they are positively and negatively selected in the light zone, they return to the dark zone for an additional round of mutation and proliferation.
Structurally similar to cytokines. Defensins are chemokines which can lyse the bacterial cell wall and chemoattract phagocytic cells.
Differentiation Associated Antigen
Shared tumor antigen specific to a particular type of cancer. Examples include CD20, PSA, tyrosinase, alphafetoprotein.
Autoantibody from PV binds here, disrupting the interkeratinocyte adhesions and causing blisters. It is a membrane protein of the cadherin family. It is Ca2+ dependent. It is present in the lower spinous layer of stratified squamous epithelium where it is involved with epidermal and keratinocyte differentiation.
Delayed Type Hypersensitivity
Type IV hypersensitivity. Antigen is presented to CD4+ T cells by the APC, steering differentiation into a Th1 cell, which secretes IFN-gamma, helping macrophages clear intracellular organisms such as TB and listeria. DTH is also the macrophage-mediated response to fungi and protozoa.
Overexpressed proto-oncogene in epithelial cancers
Why is ELISA testing used when SLE is suspected?
Test for antibodies to Smith antigen and dsDNA, which are highly specific for SLE but not very sensitive.
Present on gram positive bacteria. Encapsulate the bacteria, strongly antiphagocytic, poorly immunogenic.
F-actin is responsible for forming phagocytic cups beneath the plasma membrane around the target during phagocytosis.
Factor B
Factor B binds C3 on the bacterial surface on in the alternative pathway of complement activation. Cleaved by Factor D into Bb to make C3 convertase with C3.
Factor D
Cleaves Factor B into Factor Bb in the alternative pathway of complement activation.
Factor P
Stabilizes the C3Bb activity on the pathogen surface.
The Fc portion of the Ab is bound by NK cells, which binds to Ab-coated cells to kill them. Macrophages bind to the Fc receptor on opsonized cells and phagocytose the marked cells.
FcεI Receptor
Present on Langerhans cells, Mast cells, Basophils, and Eosinophils. This is an IgE receptor, and gets crosslinked by two molecules of IgE. Can be crosslinked with an IgG directed at the receptor or with IgE. Activates Lyn, then Syk, then leads to an increase in intracellular calcium.
Found on B cells, T cells, Monocytes, Eosinophils, etc. IgE receptor.
Fcγ Receptor
Present on DCs. With low affinity IgG antibodies the receptors must be clustered for DC activation. With high affinity IgG Abs the receptor can activate the DC monomerically. Mediates phagocytosis. Binds IgG and clusters the receptors, activing Src, then Syk which binds to the phosphorylated ITAM (like ZAP-70).
Present on myeloid cells. Can be activated with chronic stimulation. The calcium influx level will turn off NFκB signaling. If there is chronic stimulation with no LPS signaling on the B cell and no CD40L coactivation from the T cell, the myeloid cells will become anergic. FcγIIB is an inhibitory receptor. It signals through an ITIM, which recognizes SHIP and SHIP-1, binding one of these two molecules. No Btk recruited to the membrane and no PLC activation.
Follicular DC
Present antigen to B cells in the lymphoid organs. Low affinity mutants die.
Present on T cells. Interacts with Jun and MAP kinase to make AP1, which interacts with NFAT for gene transcription activation. Fos is a proto-oncogene.
Present on T cells. Clustering of CD4/TCRs activates Lck which activates Fyn. Fyn is a kinase involved in a signaling cascade.
An HIV component that packages RNA.
γδ T Cells
Play a role in oral tolerance.
HIV envelope protein that recognizes CD4 marker on T cells and monocytes.
Gram Positive Bacteria
Have a thick layer of peptidoglycan and teichoic acids, with lipids and sugars!
Gram Negative Bacteria
Have two membranes, the outer contains LPS. Endotoxin (LPS) can induce IL-1 secretion by MFs.
What molecule acts on the Hairpin Loop during TCR/BCR gene rearrangement in B and T cells?
RAG 1,2 cleave the hairpin loop. The blunt ends are joined by transesterification. The hairpin loop is nicked by Artemis.
HER2 is an overexpressed proto-oncogene in epithelial cancers and breast cancers.
Beneficial for HIV patients because they can see 15 peptides on HIV and thus mount a more effective immune response - they are slow progressors in HIV. Sucks for spondyloarthritis, however, as 95% of individuals with alkylosing spondylitis have HLA-B27, and HLA-B27 is also associated with other spondyloarthritic diseases.
Patients with HLA B35 are rapid HIV progressors. They can only see noncritical HIV parts so the MHC anchor can mutate and the virus can proliferate and invade unchecked by the immune system.
Beneficial for HIV patients because they are able to see some key peptides.
This is the chaperone that releases CLIP from MHC II and helps peptide antigen dock with MHC II. HLA-DM is homologous to MHC II.
HLA-DR (beta chain)
Present on the APC. DR1 and DR4 subtypes are relevant to Rheumatoid Arthritis and PV susceptibility (DR0401 = susceptible; DR0402 = not susceptible). RA and PV never occur together.
Present on T cells. CD28 analogue that re-activates the effector function of an already activated T cell. It is expressed on post-naive T cells.
Interepithelial lymphocytes are CD3/CD8+. Secrete IFN-γ and TNF-alpha. The HML-1 integrin directs IELs to their specific sites.
IFNs are cytokines with antiviral activity. Paracrine signaling to nearby cells by an infected cell. IFN-α and IFN-β are mainly innate immunity. IFN-γ is involved in adaptive immunity.
Which cells express IFN-α and IFN-β? What is IFN-β responsible for?
IFN-α is expressed by all cells, while IFN-β is expressed by fibroblasts. IFN-β inhibits cellular proliferation, increases NK activity, increases expression of MHC-I, and makes antiviral proteins.
Secreted by activated TH1 cells, NK cells, and CD8+ T cells. Stimulates the TH1 pathway, macrophage activation, switch to IgG isotype, increased antigen presenting by APCs. Inhibits the TH2 pathway. Increases display of MHC I and II. Leads to expression of IL-1. Increases endothelium stickiness.
Important in the mucosa, and the gut. Secreted as a dimer. B cells switch to IgA via isotype switching in germinal centers. T cell help by TH2 cells is necessary for isotype switching. IgA is resistant to intestinal proteases!!
This Ig is expressed on the cell membrane along with IgM. Pre-isotype switching. Only present on naive B cells.
Involved in allergic rxns. Isotype switching to IgE occurs in the germinal centers. Mast cells have Fc receptor for IgE and continually bind IgE. When IgE bound to Fc receptors on mast cells gets cross-linked by antigen the mast cell degranulates.
Present in the bloodstream. Isotype switch occurs in germinal centers. IgG can activate complement and OPSONIZE bacteria, etc. Pre-existing IgGs are involved in hyperacute solid transplant rejection. IgG hypersensitivity is involved in hemolytic anemia in which penicillin (or another drug hapten) attaches to RBCs, Ab attaches to the drug and lyses the cell. Can also have immune complex formation hypersensitivty (type III) in which horse serum with anti-snake venom Abs are given to a patient with a snake bite, but the body reacts to the horse serum with anti-horse Abs and immune complexes form. Called "serum sickness."
Glycosylation is essential for IgM functioning. IgM is secreted as a pentamer - low affinity but high avidity. First expressed on naive B cell membrane (along with IgD). If it reacts strongly with self Ag the B cell is usually killed by negative selection.
Igα and Igβ
Associate with the Fc portion of the mu chain, signaling the B cell to stop heavy chain rearrangement and begin light chain rearrangement. Igα and Igβ are intracellular, and have a tyrosine kinase that cross-links when the BCR is bound to Ag, starting the signaling cascade. No tyrosine kinase (Btk?) = no B cell receptor because there is NO LIGHT CHAIN REARRANGEMENT. When BCRs cluster on the cell surface in response to Ag binding there is phosphorylation of ITAMs on Igα and Igβ. Then Syk is recruited and activated.
Inhibitor of NFκB. Sequesters NFκB in the cytoplasm and prevents it from entering the nucleus and activating gene transcription.
IL-1 and TNF
These cytokines are expressed by activated MΦs. They cause anemia, fever, malaise and weight loss in patients with Rheumatoid Arthritis. They mediate inflammation and activate selectins. TNF can kill pathogens or tumors or can cause tissue damage. Stimulates phagocytosis. Costimulators for T-cell and B-cell activation. Induce fibroblast colony stimulating factor. Are responsible for some of the symptoms of septic shock: decreased myocardial contractility, decreased vascular tone, DIC.
Secreted by activated MΦs. Induced by endotoxin on Gram Negative bacteria. Also induced by TNF. IL-1 alpha and beta genes are indistinguishable in function, although the genes encode slightly different proteins. IL-1 causes fibroblast proliferation, and production of PGE2 and collagen. IL-1 causes smooth muscle proliferation. Synoviocytes and chondrocytes secrete collagenases and proteases in response to IL-1. Hepatocytes secrete acute phase reactants. Osteoclasts are activated. Thru PGE2 production, IL-1 influences the hypothalamus. IL-1 causes CRF to release glucocorticoids. The endothelium becomes sticky in response to IL-1.
Natural (endogenous) inhibitor of the IL-1 receptor which binds to the IL-1 receptor but does not transmit a signal.
Secreted by activated TH1 cells and macrophages. Causes T cell proliferation and maturation. Can cause Fas-mediated apoptosis in activated T cells who have seen a lot of antigen. Causes NK cell activation, and B cell proliferation. Induces TH1 development from TH0 cells, often via an autocrine signaling. If you remove IL-2 from an activated T cell you get apoptosis or a memory T cell.
Causes basophil degranulation, bone marrow stimulation, and eosinophil development.
Secreted by TH2 cells and mast cells. Stimulates the TH2 pathway, causes isotype switching to IgE and IgG4. Inhibits IFN-gamma activation of MΦs. Involved in allergy and asthma. Causes mast cell proliferation and degranulation via the same receptor as IL-13. In atopic dermatitis, levels of IL-4 and IL-13 are high. IL-4 drives B cell proliferation along with CD40L.
Secreted by stromal cells, TH2 cells, activated MΦs, and mast cells. It sustains plasma cells which return to the bone marrow to continually secrete small amounts of Ab to previously encountered pathogens. Stimulate normal growth of plasma cells. Can have an autocrine loop in tumors, but normally functions in an endocrine manner.
Secreted by stromal cells (in the bone marrow?) Promotes survival of stem cells committed to the B and T cell lines.
Secreted by DCs and activated MΦs. Stimulates the TH1 pathway. Stimulates DCs. Many vaccines target IL-12 TO STOP TH1 PROLIFERATION. IL-12 activates NK cells and CD8+ T cells.
Secreted by virally infected cells. Promotes NK maturation and survival.
Functions like IL-1 and TLR. Activates TH1 cells.
Functional receptor of B cells. Secreted into the serum (which includes the gut, tears, and breast milk).
Influenza Virus
Proteins in the envelope are encoded in the viral genome, and are involved in attachment of the virus to the host cell and liberation of the virus from the host cell. Genetic variability of viral envelope proteins enables the influenza virus to evade the host immune system.
Innate Immune System
Involves NK, NKT, and γδT cells. These produce IFN-γ to stimulate TH1 pathway. Tumor cells express "stress" ligands such as NKG2D, for which there are receptors on the innate immune system.
Makes nitric oxide from arginine. Stimulated by the TLR pathway.
Invariant chain
Present on APCs. Associates with the newly made MHC II and prevents cytosolic peptides from binding to the MHC II molecule as it is trafficked to the endosome. The invariant chain gets digested by acid pH proteases in the phagolysosome, leaving behind CLIP, which is then removed with help from HLA-DM, to allow the phagocytized peptide antigen to bind to MHC II and permit the MHC II-peptide complex to traffic to the cell membrane.
IP-3 increases intracellular Ca2+, which activates calmodulin, which binds to calcineurin. The calcineurin-calmodulin complex = active calcineurin phosphatase which dephosphorylates NFAT to permit its translocation into the nucleus and allows NFAT to activate gene transcription.
Immune Tyrosine Activation Motif. Located on the zeta chains of CD3. When phosphorylated, ITAMs recruit ZAP-70 kinase.
Present on T cells. Jun interacts with Fos and MAP kinase to make AP1, which interacts with NFAT to activate gene transcription. Jun is a proto-oncogene.
Junctional Diversity
Junctional diversity is generated by Artemis which creates staggered ends that are randomly chewed back.
KIR (killing inhibitory receptor)
Present on NK cells. This is a receptor for MHC-I that prevents NK from killing healthy self cells.
Lambda 5
Pseudo light chain
LPS Binding Protein (LBP)
Binds to LPS. LPS-LBP complex binds to CD14 and TLR4.
Present on T cells. This is a tyrosine kinase activated via clustering of the CD4/TCR with Fyn.
Leukotrienes C, D, and E
Important in asthma. Generated via the Arachidonic Acid pathway.
Integrin found on T cells. Binds with ICAM to cause adhesion.
Light Zone of the Germinal Center
B cells migrate to the light one from the dark zone post somatic hypermutation and proliferation. Here they get antigen from the follicular DC and interact with T helper cells. Require both signals to return to the dark zone, otherwise they undergo apoptosis.
Lipid A
Component of bacterial LPS that is highly conserved and provokes a strong inflammatory response.
Listeria is a type of bacteria that is capable of escaping from the phagosome into the cytosol.
Same as endotoxin. LPS is found on gram negative bacteria. Dendritic cells bind to LPS to distinguish self from non-self. Gram negative rods release LPS, stimulating MFs to produce TNF. Binds to LBP to form an LPS-LBP complex which binds CD14 and TLR4, thereby activating MFs.
Component of the proteasome for destruction of intracellular proteins marked with a ubiquitin tag. Cuts peptides into 9 aa fragments.
Component of the proteasome involved in the destruction of intracellular proteins marked with a ubiquitin tag. Cuts peptides into 9 aa fragments.
LTB4 (leukotriene B4)
Chemoattractant for WBCs and Eosoinophils.
Allows HIV integration. Has promoter elements and transcription factors. Transcription of HIV is decreased by IFN-gamma and TNF-alpha.
Mycobacterium tuberculosis
Type of bacteria that prevents binding of the phagosome with the lysosome and thereby evades immune detection.
DCs bind to mannose on bacteria, helps them distinguish between self and non-self.
Mannan (Mannose?) Binding Lectin
Found on bacterial surfaces. Binds to mannose instead of to Abs. Activates MASP-1 and MASP-2. This pathway is specific for bacteria.
MAP kinase
Found in T cell signaling. Interacts with jun and fos to make AP1. AP1 interacts with NFAT to activate gene transcription.
These are mannose-associated serum proteases. They are similar to C1r and C1s. They are activated by mannan binding lectin binding to mannose on the cell surface. When this occurs, they cleave C4 and C2, forming the C3 convertase, at which point this converges on the classical pathway of complement activation.
Matrix Metalloproteases
Destroy cartilage in Rheumatoid Arthritis.
Found on eosinophils. Fight parasites (not allergy). Dissolves the parasite cell wall AND the bronchial mucosa.
All nucleated cells express MHC I, while only some cells (APCs) express MHC II. MHC I binds anchor residues at position 2 and 9 of a 9 aa long recognizing pocket. There are 6 class I alleles expressed on each cell. Recognition does not require costimulatory molecules because CD8+ effector cells have already been activated by T helper cells.
MHC Class II
Binds anchor residues at positions 4 and 6. Open pocket at the ends so it can bind peptide fragments of varying length. Both the alpha chain and beta chain are variable. There are 10 different alleles because DQ and DP contribute 4 each and DR is monomeric and contributes only 2 alleles.
Mixed Lymphocyte Reaction
Response measured in the lab of a patient's response to donor MHC. If the donor cells are irradiated and we watch proliferation of the host cells, it is called a one-way MLR.
Myeloperoxidase (MPO)
Makes hypochlorus radical from hydrogen peroxide and Cl-. Found in PMN granules.
Neither gram positive nor gram negative. The outer layer has strange lipids and sugars which suppress the immune response.
N-Region Diversity
The staggered end created by Artemis receives random base pairs added by Tdt (mainly on the heavy chain).
NADPH Oxidase
All cells have NADPH oxidase. It catalyzes H2O and O2 to produce the superoxide radical. It has cytochromes which transfer electrons to reduce molecular oxygen into superoxide anion.
Encodes the negative effector protein p24 on HIV, which interacts with CD4 and MHC Class I to make the cell express less MHC Class I.
Found on T cells. It is dephosphorylated by calcineurin-calmodulin complex (the active calcineurin phosphatase) and enters the nucleus to activate gene transcription. Interacts with AP1 for transcription.
IκB sequesters NFκB in the cytosol. When IκB is phosphorylated by PKC, NFκB is allowed to enter the nucleus as a transcription factor and activate synthesis of proteins involved in immune response.
NK Cells
First response to a viral infection. If the receptor (which is NOT a TCR) is crosslinked the NK cell will kill the virally infected cell via FasL and granzymes after recognizing a part of the microbe. NK cells also have Fc receptors and kill via ADCC. Also cause of primary bone marrow graft failure. Have a KIR receptor which prevents NK cells from killing self cells which express MHC I.
The outer portion of LPS on gram negative bacteria, which is highly variable.
These are antigens shared by cancer cells and the testes during embryologic development. These antigens are re-expressed in cancer.
Extremely toxic!! Made by NO and superoxide radical.
P. aeruginosa
Opportunistic bacterial pathogen. Cleaves phagocytic receptors to avoid being taken up into the cell.
Causes cell cycle arrest when a cell is virally infected.
Papain digestion cleaves Ig into 3 pieces by cleaving above the hinge (Fc + Fab + Fab)
Causes cervical cancer.
Inhibits T cell activation.
Pepsin digestion of Ig
Cleaves Ig into 2 pieces by cleaving below the hinge (Fc + Fab2)
PGE2 (prostaglandin E2)
Produced by fibroblasts. Induced by IL-1 to simulate the hypothalamus to induce sleep, anorexia, and fever.
Picola Virus
Polio, Common Cold, SARS
PMN (Neutrophil)
Clear extracellular bacteria post-opsonization. Abs opsonize the bacteria, PMNs eat them, and then MFs eat the dead PMNs.
Encodes reverse transcriptase/polymerase and other enzymes for "the life cycle" ??? OF WHAT???
Has a large genome. Its proteins modulate the immune system.
Pre B Cell
Uses lambda 5 (surrogate light chain) and VpreB cell receptor. Then undergoes light chain rearrangement with aid of RAG1,2.
Pre T Cell
Rearranges beta chain and associates with the surrogate alpha chain.
Pro B Cell
Rearranges the heavy chain. The LC is still in its germline configuration. Uses RAG1,2 as well as Tdt, lambda 5 and VpreB.
Pro T Cell
Stem cells from the bone marrow enter the thymus as double negative cells.
Overexpressed in cancers. EGFR and HER2 are overexpressed in epithelial cancers. BCR and TCR are overexpressed in lymphomas.
Prostate Specific Antigen (PSA)
Shared tumor antigen in prostate cancer.
Pseudo TCR alpha chain that goes with the newly formed TCR beta chain when expressed on the T cell surface.
RAG1 and RAG2
Recombinase Activating Genes. These are specific to lymphocytes. They recognize RSS (recombination signal sequence of heptamer-spacer (12 or 23)-nonamer) and cleave between the gene segment and RSS. They can also be turned on for B-cell receptor editing and kappa rearrangement (if lambda rearrangement fails).
Red Pulp of the Spleen
This is the portion of the spleen where lymphocytes encounter Ag.

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