Immunologically Relevant Molecules
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| Mechanism for isotype switching? | alternative splicing of mRNA mediated by cytokines and CD40
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| Ig produced in primary (immediate) response to an antigen | IgM
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| Ig secreted as a dimer | IgA
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| Ig that crosses placenta to provide infant with passive immunity | IgG (*G*ift from mother)
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| Ig found on surface of b cells and in serum, function unknown | IgD
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| Ig that mediates immunity to worms by activating eosinophils | IgE
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| Ig that mediates type 1 hypersensitivity | IgE
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| Most effective opsonin; neutralizes bacterial toxins and viruses | IgG
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| Found in breast milk | IgA
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| Prevents attachment of bacteria and viruses to mucous membranes, but does NOT fix complement | IgA
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| Pentamer that traps free antigen out of tissue while humoral response evolves | IgM
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| Only Ig when class switching cannot occur | IgM
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| Used to detect an acute West Nile virus infection | IgM
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| First step of classic complement pathway | C1
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| deficiency of this complement component leads to recurrent infections with neisseria | C5-C9
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| Deficiency of C3 leads to increased risk of which hypersensitivity reaction? | increased susceptibility to type 3 hypersensitivity reactions
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| Cell surface proteins: T cells (general) | TCR, CD3
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| Cell surface proteins: Helper T cells | CD4, CD40L
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| Cell surface proteins: Cytotoxic T cells | CD8
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| Cell surface proteins: B cells | CD 19, 20, 21 (receptor for EBV); MHC II
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| Cell surface proteins: macrophages | MHC II, CD 14, CD16, CD40, Fc and C3b receptors
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| Cell surface proteins: NK cells | MHC I, CD16 (binds Fc of IgG), CD56 (unique marker for NK)
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| Cell surface proteins: all cells except mature RBCs | MHC I
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| Cell surface proteins: WBC, RBC, and platelets (protect against complement-mediated damage) | CD55, CD59
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| 4 exposures for which patients are given preformed antibodies (for passive immunity) | Tetanus toxin, Botulinum toxin, HBV, or Rabies virus (To Be Healed Rapidly)
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| Preemies born in winter months should be given which passive immunity vaccine every month? | RSV
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| Type I MHC is on what cells | All nucleated cells (this excludes adult RBCs)
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| Type II MHC is on what cells | Antigen presenting cells
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| Name the antigen presenting cells | Macrophages, Dendritic cells, B cells
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| MHC specific for intracellular pathogens | Type I
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| MHC specific for extracellular pathogens | Type II (Antigen presenting cells)
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| Characteristics of innate immunity | Nonspecific, Rapid, Physical barriers, Phagocytosis, Complement, Interferons, Induces inflammation
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| Characteristics of acquired immunity | Specific; Slow, then rapid; Inducible; Memory; Antibodies; B and T cells
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| Alpha & Beta interferons are produced by? | Alpha: leukocytes, Beta: fibroblasts
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| How do interferons inhibit viral replication | Place uninfected cells in "antiviral state": Alpha & beta induce a 2nd protein which degrades viral (but not host) mRNA thereby inhibiting viral protein synthesis
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| Steps to "interfere" with viruses | 1) alpha & beta interferons inhibit viral protein synth, 2) gamma-interferons incr. MHC I and II expression & antigen presentation in all cells, 3) Activate NK cells to kill virus-infected cells
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| Describe neutrophils | Formed in bone marrow, Multilobar nuclei, granules, Early defense against bacteria
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| Cells increased in pyogenic infections | Neutrophils
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| Macrophages develop in ___ as ___ | bone marrow, monocytes
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| Role of Basophils | Release of pharmacologically active substances contained within granules - Allergies
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| Role of Eosinophils | Major role against parasites - Secretion of eosinophilic granules results in damage to parasite membrane. Also involved in asthma & allergy
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| NK cells target? | cells with decreased MHC class I expression
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| 2 types of NK cell receptors | Inhibitory - recognizes MHC alpha chains; Stimulatory - recognizes cell signals
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| The 3 complement pathways are components of which immunities? | Classical: Aquired, Alternative: Innate, Lectin: Innate
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| Define complement | System of proteins that interact to play a role in humoral immunity & inflammation
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| Functions of the complement cascade | 1. Lysis of cells, bacteria, viruses, 2. Opsonization to promote phagocytosis of Ag, 3. Activation of inflammatory response , 4. Clearance of immune complexes
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| Describe the classical pathway complement cascade. | 1. C1 cleaves C4 into C4a and C4b, 2. C1 cleaves C2 into C2a and C2b, 3. C4b binds to pathogen surface , 4. C4b binds C2a, 5. C4bC2a cleaves C3 into C3a and C3b, 6. C3b binds to pathogen surface, 7. C3b cleaves C5 into C5a and C5b, 8. C5b activates MAC
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| Factors B, D and properdin are part of which complement pathway only? | alternative (properdin is important for stability of pathway)
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| MAC lyses what? | Gram(-) bacteria and viruses
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| Why are gram(+)safe from MAC? | gram(+) bacteria have thick PG coats and MAC has trouble creating pores in it
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| Activation of classic complement pathway? | IgG or IgM ("GM makes classic cars")
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| Activation of alternate complement pathway | molecules on the surface of microbes, especially LPS
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| 2 primary opsonins in bacterial defense | C3b & Ig (G or M)
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| Complement factors involved in viral neutralization | C1, C2, C3, C4
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| Complement factor involved in opsonization | C3b
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| Complement factors involved in anaphylaxis | C3a, C5a (allergic response, degranulation of eosinophils)
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| Complement factor involved in neutrophil chemotaxiS | C5a
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| Complement factors which combine to form the membrane attack complex (MAC) | C5b, C6, C7, C8, C9
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| Associated with C1 and C4 deficiencies | rheumatologic and collagen-vascular diseases
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| Associated with C3 deficiencies | severe recurrent pyogenic sinus & respiratory tract infections
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| C2 deficiency associated with? | chronic neutropenia
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| Deficiency of C1 esterase | hereditary angioedema (overactive complement)
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| Deficiency of C6-C8 | Neisseria bacteremia
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| Deficiency of decay accelerating factor (DAF) | paroxysmal nocturnal hemoglobinuria (PNH)
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| anti-nuclear | SLE & other autoimmune diseases
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| anti-dsDNA, anti-Smith | specific for SLE
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| anti-IgG | Rheumatoid arthritis (anti-IgG = "Rheumatoid Factor")
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| HLA-B27 | psoriasis, ankylosing spondylitis, Reiter's
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| HLA-DR2 | hay fever, SLE, Goodpasture's
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| Cytokine that is secreted by macrophages, stimulates just about everything, endogenous pyrogen | IL-1
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| Cytokine that stimulates growth of *all* T cells | IL-2
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| Cytokine that supports growth and differentiation of BM stem cells | IL-3 (secreted by activated T cells)
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| Cytokine that promotes growth of B cells and enhances class switching of IgE, IgG | IL-4
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| Cytokine that enhances class switching of IgA | IL-5 (also promotes differentiation of B cells, stimulates production and activation of eosinophils)
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| Cytokine that stimulates activation and production of eosinophils | IL-5
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| Cytokine that stimulates production of acute phase reactants and immunoglobulins | IL-6
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| IL that is a MAJOR chemotactic factor for PMNs | IL-8 (also, C5a)
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| Cytokine that stimulates Th2 and inhibits Th1 | IL-10 (secreted by Th2 cells themselves)
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| Cytokine that activates NK cells and Th1 cells | IL-12 (secreted by macrophages, B cells)
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| "Anticytokine" that inhibits growth and activity of T cells, counteracts effects of inflammatory cytokines, and stimulates wound healing | TGF-beta
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| Cytokine increasing IL-2 receptor synthesis by Th cells, and increases B cell proliferation | TNF-alpha (also attracts and activates PMNs, stimulates dendritic cell migration to lymph nodes)
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| Cytokine NOT produced in Job's syndrome--> "cold" staph abscesses | IFNγ (secreted by Th1 cells, stimulates macrophages)
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| Signals required for activation of helper T cells | 1) foreign Ag on MHC II recognized by TCR on Th cell; 2) costim by B7-CD28
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| Signals required for activation of cytotoxic T cells | 1) endogenously synthesized proteins on MHC I recognized by TCR; 2) IL-2 from Th cell activates cytotoxic cell
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| Cell surface proteins of Helper T cells | CD4, TCR, CD3, CD28, CD40L
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| Cell surface proteins of Cytotoxic T cells | CD8, TCR, CD3
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| Cell surface proteins of B cells | B7, CD19, CD20, CD40, MHC II
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| Cell surface proteins of Macrophages | MHC II, CD14, Receptors for Fc & C3b
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| Cell surface proteins of Natural Killer (NK) cells | Receptors for MHC I, CD16, CD56
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| Cell surface proteins of all cells except mature RBC's (all nucleated cells) | MHC I
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