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164 Cards in this Set
- Front
- Back
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Cytokine secreted by macrophages. Causes acute inflammation. Induces chemokine production to recruit leukocytes; activates endothelium to express adhesion molecules. An endogenous pyrogen.
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IL-1
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Cytokine secreted by Th cells. Stimulates growth of helper and cytotoxic T cells.
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IL-2
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Cytokine secreted by activated T cells. Suppports growth and differentiation of BM stem cells.
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IL-3
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Cytokine secreted by Th2 cells. Promotes growth of B cells. Enhances class switching to IgE and IgG.
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IL-4
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Cytokine secreted by Th2 cells. Promotes differentiation of B cells. Enhances class switching to IgA. Stimulates production and activation of eosinophils.
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IL-5
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Cytokine secreted by Th cells and macrophages. Stimulates production of acute-phase reactants and immunoglobulins.
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IL-6
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Cytokine secreted by macrophages. Major chemotactic factor for PMNs.
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IL-8
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Cytokine secreted by regulatory T cells. Inhibits actions of activated T cells. Activates Th2, inhibits Th1.
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IL-10
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Cytokine secreted by B cells and macrophages. Activates NK and Th1 cells.
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IL-12
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Cytokine secreted by Th1 cells. Stimulates mcrophages. Activates Th1, inhibits Th2.
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IFN-gamma
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Cytokine secreted by macrophages. Mediates septic shock. Causes leukocyte recruitment, vascular leak.
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TNF
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CD4, TCR, CD3, CD28, CD40L
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Helper T cells
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CD8, TCR, CD3
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Cytotoxic T cells
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IgM, CD19, CD20, CD21 (receptor for EBV,) CD40, MHC II, B7
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B cells
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MHC II, B7, CD40, CD14. Receptors for Fc and C3b.
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Macrophages
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Receptors for MH1, CD16 (binds Fc of IgG,) CD56.
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NK cells
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Lymph drainage from the stomach
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Celiac
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Lymph drainage from the duodenum and jejunum
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Superior mesenteric
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Lymph drainage from the sigmoid colon
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Colic --> inferior mesenteric
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Lymph drainage from the lower rectum, and the anal canal above the pectinate line
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Internal iliac
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Lymph drainage from the anal canal below the pectinate line
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Superficial inguinal
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Lymph drainage from the testes
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Superficial and deep plexuses --> para-aortic
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Lymph drainage from the scrotum
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Superficial inguinal
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Lymph drainage from the superficial thigh
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Superficial inguinal
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Lymph drainage from the lateral side of the dorsum of the foot
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Popliteal
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Encapsulated organisms commonly causing infections in pts w/ splenic dysfunction
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SHiNS - S pna, H flu, N meningitidis, and Salmonella
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Makes IL-2, IFN-gamma, and activates macrophages and CD8+ T cells; inhibited by IL-10
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Th1
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Makes IL-4, IL-5, IL-10, nad helps B cells make antibody (IgE > IgG); inhibited by IFN-gamma
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Th2
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IL-12 stimulaiton of a Th cell drives it to differentiate into what?
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Th1
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IL-4 stimuloation of a Th cell drives it to differentiate into what?
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Th2
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HLA subtype associated w/ hemochromatosis
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A3 (an MHC I molecule)
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HLA subtype associated w/ PAIR - Psoriasis, Ankylosing spondylitis, IBS, and Reiter's syndrome
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B27 (an MHC I molecule)
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HLA subtype associated w/ Grave's disease
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B8 (an MHC I molecule)
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HLA subtype associated w/ MS, hay fever, SLE, and Goodpasture's
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DR2 (an MHC II molecule)
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HLA subtypes associated w/ T1DM
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DR3 and DR4 (MHC II molecules)
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HLA subtype associated w/ Rheumatoid arthritis and T1DM
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DR4 (an MHC II molecule)
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HLA subtype associated w/ pernicious anemia and Hashimoto's thyroiditis
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DR5 (an MHC II molecule)
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HLA subtype associated w/ steroid-responsive nephrotic syndrome
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DR7 (an MHC II molecule)
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The only lymphocyte member of the innate immune system
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NK cells
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NK cell activity is enhanced by what?
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IL-12, IFN-beta, and IFN-alpha
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What induces NK cells to kill?
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Exposure to nonspecific activation signals on target cells, and/or absence of class I MHC on target cell surface
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Cluster of polypeptides associated w/ a TCR; important in signal transduction
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CD3 complex
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Superantigen cross-linking of the beta-retion of TCRs to the MHC class II on APCs results in release of what?
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IFN-gamma from Th1 cells, and subsequent release of IL-1, IL-6, and TNF-alpha from macrophages
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These toxins directly stimulate macrophages by binding CD14; Th cells are not involved
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Endotoxins/LPS
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Signal 1 for Th activation
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Foreign antigen presented on MHC II recognized by TCR on Th cell
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Signal 2 for Th activation
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Interaction of B7 with CD28
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Signal 1 for Tc activation
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Endogenously synthesized (viral or self) proteins presented on MHC I recognized by TCR on Tc cell
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Signal 2 for Tc activation
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IL-2 from Th cell activates Tc cell to kill virus-infected cell
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Signal 1 for B cell class switching
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IL-4, IL-5, or IL-6 from Th2 cell
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Signal 2 for B cell class switching
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CD40 ligand on Th cell binding CD40 receptor on B cell
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Deficiency of C1 esterase leads to what?
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Hereditary angioedema
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Deficiency of C3 leads to what?
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Severe, recurrent pyogenic sinus and respiratory tract infections; increased susceptibility to type III hypersensitivity reactions
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Deficiency of C5-C8 leads to what?
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Increased susceptibility to Neisseria bacteremia
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Deficiency of DAF (GPI-anchored enzyme) leads to what?
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Complement-mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria
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The primary opsonins in bacterial defence
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C3b and IgG
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Aids in clearance of immune complexes
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C3b
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MAC defends against what?
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Gram-negative bacteria
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IFNs that inhibit viral protein synthesis
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IFN-alpha and IFN-beta
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IFN that increases MHC class I and II expression, and antigen presentation in all cells
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IFN-gamma
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Half-life of antibodies acquired through passive immunity
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3 weeks
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How to T cells become anergic?
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Self-reactive T cells become nonreactive without costimulation
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RIA is used to test for what type of hypersensitivity?
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Type I hypersensitivity
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Direct and indirect Coombs is used to test for what type of hypersensitivity?
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Type II hypersensitivity
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An immune complex disease in which abys to foreign proteins are produced (takes 5 days.) ICs are deposited in membranes, where they fix complement, leading to tissue damage.
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Serum sickness (type III hypersensitivity)
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Intradermal injection of antigen induces antibodies, which form IC's in skin, causing edema, necrosis, and complement activation.
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Arthus reaction (type III hypersensitivity)
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Test for type III hypersensitivity reactions
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IF staining
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Swelling and inflammation 2-3 days after tetanus vaccination
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Arthus reaction (type III hypersensitivity)
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Sensitized T lymphocytes encounter antigen and release lymphokines, leading to macrophage activation. No aby involved.
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Type IV hypersensitivty
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Test for type IV hypersensitivity reaction
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Patch test (e.g. PPD)
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Type of hypersensitivity: hemolytic anemia
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Type II hypersensitivity
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Type of hypersensitivity: pernicious anemia
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Type II (non-cytotoxic: aby-mediated change in cell function; no complement activation.)
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Type of hypersensitivity: ITP
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Type II (anti-platelet abys)
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Type of hypersensitivity: erythroblastosis fetalis
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Type II (Rh incompatability)
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Type of hypersensitivity: acute hemolytic transfusion reaction
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Type II
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Type of hypersensitivity: rheumatic fever
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Type II
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Type of hypersensitivity: Goodpasture's syndrome
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Type II
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Type of hypersensitivity: Bullous pemphigoid
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Type II (anti-BP abys; IF at DEJ)
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Type of hypersensitivity: Pemphigus vulgaris
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Type II (anti-desmoglein abys; reticular IF pattern)
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Type of hypersensitivity: Grave's disease
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Type II (non-cytotoxic: aby-mediated change in cell function; no complement activation.)
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Type of hypersensitivity: Myasthenia gravis
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Type II (non-cytotoxic: aby-mediated change in cell function; no complement activation.)
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Type of hypersensitivity: SLE
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Type III
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Type of hypersensitivity: Rheumatoid arthritis
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Type III (RF is an anti-IgG aby)
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Type of hypersensitivity: PSGN
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Type III
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Type of hypersensitivity: PAN
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Type III
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Type of hypersensitivity: hypersensitivity pneumonitis (e.g. farmer's lung)
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Type III
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Type of hypersensitivity associated w/ vasculitis and systemic manifestations
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Type III
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Type of hypersensitivity associated w/ local disease where antigen is found
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Type II
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Type of hypersensitivity: T1DM
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Type IV hypersensitivty
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Type of hypersensitivity: MS
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Type IV hypersensitivty
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Type of hypersensitivity: GBS
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Type IV hypersensitivty
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Type of hypersensitivity: Hashimoto's thyroiditis
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Type IV hypersensitivty
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Type of hypersensitivity: GVHD
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Type IV hypersensitivty
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Type of hypersensitivity that does not involve antibodies
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Type IV hypersensitivty
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Autoantibodies specific for SLE
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Anti-dsDNA, anti-Smith
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Autoantibodies associated with drug-induced lupus
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Anti-histone
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Autoantibodies associated with RA
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RF (anti-IgG)
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Autoantibodies associated with localized Scleroderma (CREST)
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Anticentromere
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Autoantibodies associated with primary biliary cirrhosis
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Antimitochondrial
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Autoantibodies associated with celiac disease
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Antigliadin and antiendomysial
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Autoantibodies associated with Pemphigus vulgaris
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Anti-desmoglein
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Autoantibodies associated with Hashimoto's thyroiditis
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Antimicrosomal and antithyroglobulin
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Autoantibodies associated with polymyositis and dermatomyositis
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Anti-Jo-1
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Autoantibodies associated with MCTD
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Anti-U1 RNP (ribonucleoprotein)
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Autoantibodies associated with autoimmune hepatitis
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Anti-smooth muscle
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Autoantibodies associated with T1DM
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Anti-glutamate decarboxylase
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Autoantibodies associated with Wegener's granulomatosis
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c-ANCA
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Recurrent bacterial infections after 6 months due to opsonization defect; normal pro-B cells, decreased maturation/number of B cells, decreased Ig's of all classes
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Bruton's agammaglobulinemia
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Defective CD40L on helper T cells = inability to class switch
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Hyper-IgM syndrome
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Severe pyogenic infections early in life. Increased IgM, decreased IgG, IgA, and IgE.
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Hyper-IgM syndrome
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Defect in isotype switching leading to deficiency in specific classes of Ig's
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Selective Ig deficiency
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Sinus and lung infections, milk allergies and diarrhea, anaphylaxis on exposure to blood products
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IgA deficiency (failure to mature into plasma cells --> decreased secretory IgA)
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Can be acquired in 20's-30's. Increases risk of autoimmune disease, lymphoma, and sinopulmonary infections. Normal number of B cells, but decrease in plasma cells and Ig's
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CVID (defect in B cell maturation from many causes)
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Decreased Th1 response --> disseminated mycobacterial infections
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IL-12 receptor deficiency (labs show decreased IFN-gamma.)
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Secreted by macrophages and B cells; stimulates NK and Th1 cells
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IL-12 (IL-12 receptor deficiency --> disseminated mycobacterial infections)
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Th cells fail to produce IFN-gamma to recruit PMNs to site
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Hyper-IgE syndrome (Job's syndrome) - FATED: coarse Facies, cold (non-inflamed) Staph Abscesses, retained primary Teeth, increased IgE, and Derm problems (eczema)
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Coarse Facies, cold (non-inflamed) Staph Abscesses, retained primary Teeth, increased IgE, and Derm problems (eczema)
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Hyper-IgE syndrome (Job's syndrome/hyper-IgE syndrome): FATED. Th cells fail to produce IFN-gamma to attract PMNs.
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What defect causes chronic mucocutaneous candidiasis?
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T-cell dysfunction
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4 B cell immune deficiency disorders
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Bruton's agammaglobulinemia, Hyper-IgM syndrome, Selective Ig deficiency, and CVID
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4 T cell immune deficiency disorders
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Thymic aplasia (DiGeorge,) IL-12 receptor deficiency, Hyper-IgE syndrome (Job's,) and chronic mucocutaneous candidiasis
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3 immune deficiencies with disorders of both B and T cell function
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SCID, ataxia-telangiectasia, and Wiskott-Aldrich
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3 immune deficiencies of phagocyte function
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Leukocyte adhesion deficiency (type I,) Chediak-Higashi, and CGC
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3 causes of SCID
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Defective IL-2 receptor (X-linked - MCC); adenoisine deaminase deficiency; failure to synthesize MHC II antigens
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Recurrent viral, bacterial, fungal, and protozoal infections due to both B and T cell deficiency. Tx: BMT (no allograft rejection.)
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SCID, ataxia-telangiectasia, and Wiskott-Aldrich
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SCID due to decreased T cell activation
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IL-2 receptor deficiency (MCC; X-linked)
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Why does adenosine deaminase deficiency cause SCID?
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High levels of adenine is toxic to B and T cells; decreased dNTPs inhibit DNA synthesis (less important)
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Cerebellar defects, spider angiomas, IgA deficiency
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Ataxia-telangiectasia (defect in DNA repair enzymes)
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Triad of ataxia-telangiectasia
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Cerebellar defects, spider angiomas, IgA deficiency
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Thrombocytopenic purpura, infections, and eczema
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Wiskott-Aldrich syndrome (X-linked; progressive deletion of B and T cells)
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Ig levels seen in Wiskott-Aldrich syndrome
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Increased IgE and IgA, decreased IgM)
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Defect in LFA-1 integrin (CD18) protein on phagocytes
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LAD-1 (causes neutrophilia; recurrent bacterial infections, absent pus formation, delayed separation of the umbilicus)
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Neutrophilia, recurrent bacterial infections, absent pus formation, delayd separation of the umbilicus
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LAD-1 (defect in LFA-1 integrin/CD18 on phagocytes)
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AR; defect in microtubular function resulting in decreased phagocytosis
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Chediak-Higashi syndrome
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Recurrent pyogenic infections by Staph and Strep; partial albinism, peripheral neuropathy
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Chediak-Higashi syndrome
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Lack of NADPH oxidase --> decreased ROS and absent respiratory burst in PMNs
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CGD
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Increased susceptibility to catalase-positive organisms (S aureus, E coli, Aspergillus)
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CGD
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Test for CGD
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Nitroblue tetrazolium dye reduction test (negative in CGD)
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Preformed antidonor antibodies in transplant recipient --> type II hypersensitivity
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Hyperacute transplant rejection
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T cells react against foreign MHCs weeks after transplantation. Reversible w/ immunosuppressants (cyclosporine or OKT3/muromonab-CD3)
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Acute transplant rejection
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T cell and aby-mediated vascular damage (obliterative vascular fibrosis) months to years after transplantation. Irreversible. CTL destruction of cells w/ foreign class-I MHC molecules.
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Chronic transplant rejection
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Sx of GVHD
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Maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea
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Binds to cyclophilins --> inhibits calcineurin --> blocks differentiation/activation of T cells -- > prevents production of IL-2 and its receptor
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Cyclosporine
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Uses of cyclosporine
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Post-transplantation; some autoimmune disorders
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Immunosuppressant that predisposes pts to viral infections and lymphoma; nephrotoxic (preventable w/ mannitol diuresis)
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Cyclosporine
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Binds FK-binding protein, inhibiting secretion of IL-2 and other cytokines
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Tacrolimus (FK506)
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Use of tacrolimus (FK506)
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Post-transplantation
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Immunosuppressant that causes nephrotoxicity, peripheral neuropathy, HTN, pleural effusion, and hyperglycemia
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Tacrolimus (FK506)
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Antimetabolite precursor of 6-MP that interferes w/ metabolism and synthesis of nucleic acids. Toxic to proliferating lymphocytes.
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Azathioprine
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Uses of azathioprine
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Kidney transplantation, autoimmune disorders (e.g. glomerulonephritis, hemolytic anemia)
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Immunosuppressant that causes BM suppression. Toxic effects increased by allopurinol.
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Azathioprine (the active metabolite mercaptopurine is metabolized by xanthine oxidase - thus the effects of allopurinol.)
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Monoclonal aby that binds CD3 (epsilon chain) on T cells
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Muromonab-CD3 (OKT3)
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Uses of muromonab-CD3 (OKT3)
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Kidney transplantation
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Immunosuppressant that causes cytokine release syndrome, hypersensitivity
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Muromonab-CD3 (OKT3)
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Binds to mTOR. Inhibits T-cell proliferation in response to IL-2.
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Sirolimus (rapamycin)
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Use of sirolimus (rapamycin)
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Kidney transplantation (combined w/ cyclosporine and corticosteroids)
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Immunosuppressant that causes hyperlipidemia, thrombocytopenia, and leukopenia
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Sirolimus (rapamycin)
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Inhibits de novo guanine synthesis and blocks lymphocyte production
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Mycophenolate mofetil
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Monoclonal aby with high affinity for the IL-2 receptor on activated T cells
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Daclizumab
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Aldesleukin
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Recombinant IL-2 cytokine used for renal cell carcinoma, metastatic melanoma
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Filgrastim
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Recombinant GCSF used in recovery of BM
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Sargramostim
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Recombinant GMCSF used in recovery of BM
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Recombinant cytokine used in tx of HBV, HCV, Kaposi's sarcoma, leukemias, and malignant melanoma
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IFN-alpha
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Recombinant cytokine used in tx of MS
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IFN-beta
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Recombinant cytokine used in tx of CGD
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IFN-gamma
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Oprelvekin
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Recombinant IL-11 cytokine usd in thrombocytopenia
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