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74 Cards in this Set
- Front
- Back
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Innate immunity
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Receptors that recognize pathogens are germline encoded; response to pathogens is fast and nonspecific. No memory
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Adaptive immunity
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Receptors that recognize pathogens undergo VDJ recombination during lymphocyte development. Response is slow to first exposure, but memory response is faster and more robust
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MHC I
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found on all nucleated cells; binds to CD8
viral immunity |
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MHC II
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found only on APCs
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IgG
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main antibody in secondary response; most abundant; fixes complement, crosses placenta, opsonizes bacteria, neutralizes bacterial toxins and viruses; half life is 21 days
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IgA
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prevents attachment of bacteria and viruses to mucous membranes; does not fix complement; monomer or dimer; found in secretions
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IgM
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Produced in primary response to an antigen; fixes complement but does not cross the placenta; on B cells; monomer or pentamer
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IgD
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found on surface of B cells
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IgE
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mediates type I HS- induces release of mediators from mast cells and basophils when exposed to allergen
mediates immunity to worms |
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IL1
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secreted by macrophages; stimulates T and B cells, neutropils, fibroblasts and epithelial cells to grow, differentiate or synthesize specific proteins
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IL2
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secreted by Th1 cells; stimulates growth of helper and cytotoxic T cells
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IL3
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secreted by activated T cells; supports the growth and differentiation of bone marrow stem cells; has function similar to GM-CSF
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IL4
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secreted by Th2 cells; promotes growth of B cells; makes IgE and IgG
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IL5
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secreted by Th2 cells; promotes differentiation of B cells; makes IgA; stimulates production and activation of eosinophils
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IL6
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secreted by Th cells and macrophages; stimulates production of acute phase reactants and immunoglobulins
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IL8
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major chemotactic factor for neutrophils (along with C5a)
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IL10
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secreted by Th2 cells. stimulates Th2 while inhibiting Th1
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IL12
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secreted by B cells and macrophages. Activates NK and Th1 production
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gamma IFN
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secreted by Th1 cells, stimulates macrophages
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TNF-alpha
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secreted by macrophages; increases IL2 receptor synthesis by Th cells; increases B cell proliferation, attracts and activates neutrophils; stimulates dendritic cell migration to LN
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Acute phase reactants
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IL1, IL6, TNF alpha
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Th1 cell
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induced to form by IL12; produce IL2, IFN IL12, and activates macrophages and CD8 cell (cytotoxic T)
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Th2 cell
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induced to form by IL4; produce IL4, IL5, IL10 and help B cells make antibody
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Helper T cell surface proteins
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CD4, TCR, CD3, CD28, CD40L
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Cytotoxic T cells surface proteins
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CD8, TCR, CD3
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B cells surface proteins
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IgM, IgD, B7, CD19, CD20, CD40, MHCII, CD21
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Macrophage surface proteins
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MHCII, CD14, Receptors for Fc and C3b, CD16
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NK cells
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receptors for MHCI, CD16, CD56
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Decay accelerating factor
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CD55, 59- on wbc, rbc, and platelets, protect against complement damage
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Alternative complement pathway stimulated by
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microbial surfaces
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Lectin pathway stimulated by
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microbial surfaces
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Classic pathway stimulated by
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antigen-antibody complexes
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C1, C2, C3, C4
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viral neutralization
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C3b
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opsonization
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C3a, C5a
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anaphylaxis
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C5a
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neutrophil chemotaxis
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C5b-9
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cytolysis by MAC
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Def of C1 estarase inhibitor
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hereditary angioedema
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Def of C3
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severe recurrent pyogenic sinus and respiratory tract infections
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Def C6-C8
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Neisseria bacteremia
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Def of DAF
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paroxysmal nocturnal hemoglobinuria
dx with HAMS (RBC lysis at low ph) or flow cytometry for CD55, 59 |
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What do IFNs do
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induce the production of a second protein that inhibits viral protein synthesis by degrading viral mRNA; also activate NK cells to kill virus infected cells
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alpha and beta IFN
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inhibit viral protein synthesis
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gamma IFN
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increase MHC I and II expression and antigen presentation in all cells
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Active immunity
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induced after exposure to foreign antigens; slow onset; long lasting protection
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Passive immunity
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based on receiving preformed antibodies from another host; rapid onset; short life span of antibodies
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Give passive immunity for
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Tetanus, Botulinum, HBV, Rabies, RSV exposure
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Type I HS
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antigen cross links IgE on presenstized mast cells, triggering release of vasoactive amines; RAPID
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Type II HS
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antibodies against self- IgM, IgG bind to antigen leading to lysis by complement or phagocytosis
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Type III HS
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Immune complex mediated; deposit in tissues and activate immune system
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Type IV HS
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delayed type- sensitized T lymphocytes encounter antigen and then release lymphokines- leads to macrophage activation
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Type I HS examples
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anaphylaxis, allergic rhinitis, asthma, hives
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Type II HS examples
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hemolytic anemia, Idiopathic TCP, erythroblastosis fetalis, rheumatic fever, goodpastures, bullous pemphigoid, graves, myasthenia gravis
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Type III HS examples
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lupus, RA, polyarteritis nodosum, PSGN, serum sickness, arthus reaction, HS pneumonitis
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Type IV HS examples
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T1DM, MS, Guillain Barre, Hashimotos, GVHD, PPD, contact dermatitis
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B27
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Psoriatic arthritis, ankylosing spondylitis, inflammatory bowel disease, reiter's syndrome
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hyper acute rejection
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antibody mediated due to the presence of preformed antibodies on donor; immediate
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acute rejection
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cell mediated due to cytotoxic T lymphos reacting against foreign MHCs; occurs weeks after; reversible
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chronic rejection
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antibody mediated vascular damage; months to years after; irreversible
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GVHD
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T cells mediated; bone marrow graft has new immune system that attacks the host
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displayed only by helper T cells
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CD4
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displayed only by cytotoxic T cells
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CD8
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found on all T cells (except NK)
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CD3
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used to ID B cells
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CD19, 20, 21
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Bruton's agammaglobulinemia
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X linked (boys), B cell def- defective tyrosine kinase gene
low levels of ALL Igs recurrent bacterial infections after 6 mos |
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Thymic aplasia (DiGeorge)
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3rd and 4th pouches fail to develop- no thymus - no T cells, no PTH - low Ca, tetany
congenital defects in heart and great vessels, recurrent viral, fungal and protozoal infections 22q11 deletion |
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Chronic mucocutaneous candidiasis
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T cell dysfunction against C albicans
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SCID
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adenosine deaminase deficiency; recurrent infections
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Wiskott Aldrich Immunodeficiency
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TCP, eczema, recurrent pyogenic infections, no IgM vs capsular bacteria, high IgA
X linked |
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Ataxia telangiectasia
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IgA def; cerebellar ataxia; spider angiomas
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Selective Ig def
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IgA is most common, usually asymptomatic
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Chronic granulomatous disease
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lack of NADPH oxidase activity- impotent phagocytes
opportunistic infections- S aureus, E Coli, Aspergillus prophylactic TMP-SMX |
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Chediak Hegashi
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defective macrophages- microtubular and lysosomal
see giant granules in neutrophils recurrent staph/streph infections partial albinism |
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Job's sydrome
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no Th cell production of IFN gamma; neutrophils fail to respond to chemotactic stimuli
high levels of IgE recurrent staph abscesses |
