lecture 26 ansari
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| adaptive immune system | T and B lymphocytes with greater specificity in their receptors to catch many types of antigens; usually is the cause along with other mononuclear cells of chronic inflammation
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| innate immune system | is non-specific and uses germline receptors like PAMPs and TLRs to catch invading pathogens --> NK cells, dendritic cells, phagocytes, etc. Responsible for the short-lived acute inflammation response
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| conductor vs executor of adaptive immunity | conductor - CD4+ T cells that signal other immune cells to get working
executor - CD8+ T cells that kill things
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| type I hypersensitivity reactions | IgE-mediated allergic rxns in a pre-sensitized host. Mast cells with specific IgE will react when they come in contact with invading Ag again, need Th2 cell help; cause asthma exacerbation, urticaria, etc from histamine release
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| atopy | describes the tendency of an individual to be prone to type I hypersensitivity reactions, that is mast cell degranulation causing urticaria, etc when exposed to various Ags in environment
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| examples of type I hypersensitivity reactions | atopic bronchial asthma, atopic dermatitis, hives/urticaria, allergic rhinitis or conjunctivitis, hay fever, even anaphylaxis
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| type II hypersensitivity reactions | antibody-mediated; Abs bind to EC matrix or RBCs (in hemolytic anemia) with subsequent destruction by opsonization (phagocytosis) or complement activation/lysis
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| examples of type II hypersensitivity reactions | Grave's dz, myasthenia gravis, pemphigus vulgaris, hemolytic dz of the newborn, Goodpasture syndrome
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| Goodpasture syndrome | antiglomerular BM and lung alveolar antibody deposition causes rapidly progressive glomerulonephritis and pulmonary hemorrhage. remember LINEAR PATTERN OF AB AND COMPLEMENT DEPOSITION
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| type III hypersensitivity reactions | mediated by deposition of immune complexes in extravascular sites or vessel walls. injury through complement activation or recruitment of neutrophils or monocytes. formation of immune complexes in the blood is not necessarily abnormal!!
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| examples of type III hypersensitivity reactions | polyarteritis nodosa: Hep B virus antigens;
SLE: Abs against DNA and nuclear proteins;
serum sickness (horse antithymocyte globulin) and arthus rxns
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| remember LUMPY-BUMPY pattern of Ab and complement deposition | type III hypersensitivity reactions
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| type IV hypersensitivity reactions | cell-mediated delayed-type hypersensitivity over the course of days-wks; initiated by Ag-activated CD4+ T cells that activate macrophages and bring in mononuclear infiltrate. CD8+ T cells do cytotoxicity directly
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| examples of type IV hypersensitivity reactions | contact dermatitis, skin testing (PPD), type 1 DM, MS, RA, graft rejections
TB infections causing granuloma formation
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| systemic lupus erythematosus (SLE) | Chronic, remitting-relapsing prototypical systemic autoimmune illness affecting predominantly kidney, joints, skin and serosal membranes;
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| screening for presence of _______ is the first step to diagnosis SLE | anti-nuclear antibody (ANA)
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| more specific tests for definitive dx of SLE | anti-dsDNA antibody and anti-Smith antibody
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| screening for presence of _______ leads to dx of Sjogren's syndrome | anti-SS-A and anti-SS-B antibody tests (anti-ribonucleoprotein antibodies)
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| screening for presence of _______ leads to dx of systemic sclerosis | anti-Scl-70
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| pathogenesis of SLE | pt already has decreased lymphocyte tolerance, stresses like UV radiation and immunological factors cause cytolysis of cells, increased nuclear protein load leads to Ab formation against them --> immune complexes form on various organs (type III)
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| cause of death in many pts with lupus | renal manifestations - deposition of DNA-anti-DNA complexes in glomerulus (class IV, diffuse proliferative GN is worst prognosis)
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| Sjogren's syndrome | lymphocytic infiltration and fibrosis of salivary glands and lacrimal glands causing chronic dry eyes and xerostomia; usually associated with other autoimmune dz like SLE or RA (secondary form); ANA usually (+)
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| scleroderma | abnormal accumulation of fibrous tissue in skin and other organs, either diffuse or limited type; anti-DNA topoisomerase I antibodies (Scl-70) or anti-centromere antibodies
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