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Immunology Block II

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asuliman's version from 2016-06-21 18:28

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Located on macrophage and B Cells and interacts with CD40L and causes release of IFN-γCD40
Located on activated T Cell, interacts with CD40 and causes release of IFN-γ and Allows for class switching on B cellsCD40L
Released from macrophages, helps TH1 differentiation and causes IFN-γ productionIL-12
State of unresponsivenessAnergy
Low affinity IL-2 receptor on T cellsIL-2Rβγc
High affinity IL-2 receptor on T CellsIL-2Rαβγc or CD25
Made by TH2 Cells, causes B cell switching to IgEIL-4
Stimulates B cell growthIL-4
Inhibit macrophages activation and TH1 mediated reactionsIL-4
Autocrine GF for TH2IL-4
Induces STAT 6 → GATA 3 → TH2IL-4
Made by TH2 Cells, causes recruitment and activation of eosinophils & IgA class switchingIL-5
Stimulates B-cells differentiationIL-5
Inhibit macrophages activation and TH1 mediated reactionsIL-5
Made by T helper cells Inhibition of T cell activation , down-regulated T cell proliferationTGF-β
Present on T Cells and is an integrin that bind to ICAM-1 on APC so they adhereLFA-1
Present on APC to bind to LFA-1 on T Cells so they adhere ICAM-1
Present on T cells and bind B7 on APCsCD28
Present on T cells and is a inhibitory receptor. Shuts off T cell response and have higher affinity for B7 on APC than CD28. Controls autoreactive T cells, mediates Ag specific apoptosis CTLA-4
Present on T Cells, binds to VCAM-1 on the endothelium VLA-4
Present in endothelium and binds VLA-4 on T cellsVCAM-1
Recognize Ag on dendritic cells, macrophages. Class II MHCT Helper Cells
Binds to CD4+ → activates STAT4 (TF) →TH1 → IFNγ → induces Tbet →Activates CTL IL-12
Release Granzymes and perforin to activate apoptotic pathways. Perforin allows granzymes to get in and activate caspases CTLs
Expressed on target cell for FasL on CTL to recognize and induces apoptosis. Also expressed by self reactive T cells, so if there is a mutation = autoimmune disorderFas (CD95)
Expressed on CTL and binds to target cell with Fas and induces apoptosisFasL
Produce TH17 and TH22TH17
Produced by TH17 , Recruits neutrophils to site of inflammation and causes production of other cyto/chemoIL-17
Produced by TH17, maintains epithelial barrier function in intestineIL-22
Produced by TH2IL-13
Opsonin , activate complement, ADCC IgG recognized by FcγRIIIA on NK cells IgG1
Opsonin, activate complement , ADCC: IgG recognized by FcγRIIIA on NK cellsIgG3
Lymphotoxin, with TNF activate neutrophils and stimulates inflammation LT
Along with LT activate neutrophils and stimulates inflammationTNF
Peaks at 48hrs, requires TH1 cells. Type IV hypersensitivityDHT
In Type IV DTH, an increase in fibrous element in tissues, loss of elasticity Induration
TH2 required. Ag recognition →Ab cross-linking on B cell →increases expression of Class II MHC & B7 → T cell recognizes MHC II & B7 = TH2 activation → Expression of CD40L on T cell. →Interaction between CD40 and CD40L (allows for class switching) → B cells express receptors for cytokines → Receptors recognize cytokines released by TH2 = B cell differentiation, memory and class switchingThymus dependent Ag B cell activation
Innate immunity, No memory no isotype switching (so all IgM), no somatic mutations and no affinity maturation Thymus independent Ag B cell activation
Type 2 complement receptor, recognizes C3d and activates B cellsCR2
Activates B cell and prepares it for interaction with the T cellC3d
CD40L is missing and thus class switching can’t occur. Increased levels of IgM. Causes recurrent respiratory infections. Primarily affects males X linked Hyper IgM Syndrome
Multiple alleles exist for some isotype gene that encode subtle amino acid differences = polymorphismAllotype
They are antigenic but lack immunogenicity but chemically coupled with another molecule == immunogenic hapten-carrier conjugateHapten
Constant region determinants that collectively define each heavy chain and light chainIsotype
Individual determinant of the variable region – specific for a given AgIdiotype
Additional proteins that is required to make a dimer of IgA and stably form a pentomer of IgMJ chain
Present on Macrophages, neutrophils, eosinophils and binds IgG1 and IgG3 = phagocytosisFcγRI
Opsonin recognized by CR1, causes phagocytosis. CR1 also recognizes C4b. Activates the alternative pathway. If on surface of the microbe, it binds factor B and forms C3 convertaseC3b
Present on macrophages, neutrophils, eosinophils, platelets recognizes IgG= phagocytosis FcγRIIA
Present on B lymphocytes, recognizes IgG = feedback inhibition of B cellsFcγRIIB
Present on monocytes, macro, neutrophils, eosinophils recognizes IgA = phagocytosis FcαRI
Induces base pair changes into the V(D)J region of Ig variable regionsSomatic Hypermutation
Suppresses cell-mediated immune responsesCortisone
IgM and IgG binds C1 and C3 convertase is C4b2aClassical Pathway
Microbe and C3b bind C3 convertase is C3bBbAlternative Pathway
MBL binds terminal mannose sugars C3 convertase is C4b2aLectin Pathway
Potent anaphylatoxinC5a
AnaphylatoxinC3a
AnaphlatoxinC4a
C3 Convertase of Alternative complement pathway and cleaves C3 → C3b and C3aC3bBb
C3 Convertase of Classical and lectin complement pathways and cleaves C3 into C3b and C3a C4b2a
C5 Convertase of Alternative complement pathway and cleaves C5 → C5a and C5bC3bBbC3b
C5 Conversase of Classical and lectin complement pathways and cleaves C5→ C5a and C5b C4b2aC3b
Forms the membrane-attack complex in complementC5b
Protein in the alternative complement pathway that cleaves Factor B when it is bound to C3b Factor D
Protein in the alternative complement pathways that stabilized the C3 convertase on microbial surfacesProperdin
Component of the MAC; binds to C5b and accepts C7C6
Component of the MAC; binds C5b, 6 and inserts into lipid membraneC7
Component of the MAC; binds C5b,6,7 and initiates binding and polymerization of C9C8
Component of the MAC; binds C5b ,6,7,8, and polymerizes to form membrane pores. Deficiency leaves to increases susceptibility to Neisseria infections C9
Protein that displaces Bb from C3b in the C3 convertase in the alternative complement pathwayDAF
Prevents the assembly of the C1 complex, (C1q, C1r, and C1s)= blocks activation of the classical pathwayC1 Inhibitor
Membrane cofactor protein, a cofactor for (Factor I)= the cleavage of C3b and C4bMCP
Cleaves C3b and C4bFactor I
Causes dissociation of alternative pathways C3 convertase & Co-factor of Factor I cleavage of C3bFactor H
Increased susceptibility to recurrent infections, autoimmune disordersC3 deficiency
Increased incidence of immune complex diseases such as SLE (systemic lupus erythematosus)C2 & C4 deficiency
Attract leukocytes to site of infectionChemokines
Protect against viral infectionsType I IFNs: α & β
Alpha chain of the IL-2 receptor. Present on Activated B and T cells. Has a high affinity for IL-2 CD25
Secreted by TH1 and increases activity of macrophages and activates CTLs. Stimulates increase in IL-12 IFN- γ
Made by TH1 cells Activates TH , B , TC, NK cellsIl-2
Released from macrophages, mediates host inflammatory responses, activates TH cells Il-1
Can express allele from only 1 parent, B cells do this and this helps ensure that each cells expresses receptors of a single specificity. Ex: Rearrangement of Heavy-chain Allelic Exclusion
Nucleotides that fill in overhanging nucleotides. Using palindromic sequences P nucleotides
Removes nucleotides Exonucleases
Catalyzes random addition of nucleotides that are not part of the germline to junctions called N regions TdT
Even more diversity due to changes in nucleotide sequences added to junctions of V, D, J by Tdt enzyme Junctional diversity
The recombination of many V,D,J regions allows for a diversity of Ag receptors Combinatorial diversity
Activate VDJ recombinase, flank sequences and bring them together. Only expressed in immature b/t cells RAG1 & RAG2
Only present in heavy chain and TCR β chainD segment
Production of diverse Ag receptors, D with J then DJ with V = variable segment, spliced onto C region that encodes for µ = µ heavy chain = IgM (1st Ig protein synthesized) **mediated by VDJ recombinase Somatic Recombination
Immature T Cells and B Cells selected against those who recognize self strongly. B cells can reactivate the VDJ recombinase to generate a 2nd light chain to see if it will survive Negative Selection
Immature T cells selected to recognize self MHC molecules weakly if not apoptosis, B cell also not MHC Positive Selection
Weak recognition of class I MHC and peptide = positive selectionMature CD8+ T Cell
Weak recognition of class II MHC and peptide = positive selectionMature CD4+ T Cell
Contain both IgM and IgD Mature B Cell
Expresses both β and α chains , double positive CD4+ CD8+ Immature T Cell
Expresses both heavy and light chains (IgM) Immature B Cell
Expresses β chain and pre-Tα chainPre T cell
Expresses heavy chain and surrogate light chainPre B cell
Double negative (CD4- CD8-)Pro T Cell
Expresses Igα and IgβPro B Cell
Stimulate survival & proliferation of progenitor T cells before they express Ag receptors IL-7
Present on NK cells and recognizes Ag on IgGFCR3A receptor
Secreted as a pentamer – J chain (10 Ag binding sites) –Highest avidity, lowest affinity, main Ab produced Naïve B cell Ag receptor, complement activation** IgM
Secretes as a monomer - hidge ( 2 Ag binding sites), most stable and abundant, opsonization, complement activation, ADCC, passes placenta, feedback inhibition of B cells IgG
In naïve B cell Ag receptor IgD
Usually secreted as a dimer – hinge, J chain (4 Ag binding sites) – mucosal immunity, Neutralization **in breast milk Can opsonize as well IgA
Strength of interaction between Ag and Ab when multiple epitopes interact. IgM has greatest avidity Avidity
Ab produced against 1 Ag can bind another structurally similar Ag Cross-Reaction
Affinity increases with repeated stimulation. Done by somatic hypermutation, in germinal centers by AID Affinity maturation
Strength at which 1 Ag binds on Ab. Measured in Kd ( ↓Kd = ↑affinity) TCR is low Affinity
IgM and IgD (do this by alternative splicing) – can undergo class switching Receptors on naïve B cells
Breaks into 2 Fab and 1 Fc monovalent, Capable of Ag bindingPepain
Breaks into F(ab’)2 bivalent capable of Ag binding and bridging Pepsin
Allows 2 Fab regions to move independently and simultaneously bind antigen epitopes Hinge on Ab
Only part of heavy chain, required for effecter function Fc region of Ab
Includes whole light chain and part of heavy chain, required for antigen binding Fab region of Ab
Most variable hypervariable region that is located at junction of V&C regions, helps in Ag binding. Also present on TCR as well CDR3
1 variable and 3-4 constant regions, 3 hypervariable regions (CDRs). µ , α , δ , ε (for classes Ab heavy chain
1 variable and 1 constant region. Either κ or λAb light chain
A localized region on the surface of an Ag that is capable of elicting an immune response Epitope/determinant
Signaling molecule on TCR complex 2 homodimersζ
Signaling molecule on TCR complex 2 heterodimers CD3
Signaling molecule on Ab Igβ
Signaling molecule on Ab Igα
CD3 and ζ TCR Complex
Composed of α & β chains (1V and 1 C each) 5-10% have γ & δ chains (recognize non-protein too) T cell receptor
Igα & Igβ, transmits signals and causes B cell activation BCR complex
Conserved portions, required for effecter function Constant region on Ab
Ag recognizing portion of receptor, varies between clones. Each have 3 hypervariable regions Variable region on Ab
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