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CD, Ig, & Cytokines

Immunologically Relevant Molecules

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