pathology of autoimmune disease
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| cytokines | soluble proteins secreted by lymphocytes, monocytes-macrophages, and NK cells, as well as other cell types; are similar to dendritic cells of lymphoid tissue in that they express HLA class II antigens and are antigen presenting cells
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| IL-1 | from monocytes, macrophages; stimulates T cell proliferation and IL-2 production
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| IL-2 | macrophages, T cells and NK cells; stimulates proliferation of T cells, B cells, and NK cells; activates monocytes
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| IL-3 | T cells; acts as growth factor for tissue mast cells and hematopoietic stem cells
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| IL-4 | T cells; promotes growth of B cells and T cells; enhances expression of HLA class II antigens
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| IL-5 | T cells; promotes end stage maturation of B cells into plasma cells
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| IL-6 | T cells, monocytes; promotes maturation of B and T cells; inhibits growth of fibroblasts
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| IFN ALpha | B cells and macrophages; has antiviral activity
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| IFN beta | fibroblasts; has antiviral activity
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| IFN gamma | T cells and NK cells; has antiviral activity; activates macrophages; enhances expression of HLA class II antigens
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| TNF alpha | macrophages, T cells, and NK cells; stimulates T cell proliferation and IL-2 production; cytotoxic to some tumor cells
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| TNF beta | T cells; stimulates T cell proliferation and IL-2 production; cytotoxic to some tumor cells
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| Type 1 hypersensitivity | antigen reacts with IgE bound to surface of basophils or tissue mast cells, causing degranulation with release of histamine and other substances, many of which are vasoactive, smooth muscle spasm-inducing, or chemotactic
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| Type 1 hypersensitivity | hay fever; allergic asthma; hives; anaphylactic shock
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| type 2 hypersensitivity | antibodies react with antigens that are intrinsic components of cell membrane or other structures, such as basement membranes, resulting in direct damage, compliment mediated cytotoxicity; also may be caused by inactivation of cell-surface receptors by an
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| type 2 hypersensitivity | warm antibody autoimmune hemolytic anemia;hemolytic disease of the newborn; goodpasture syndrome; graves disease
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| type 3 hypersensitivity | insoluble complement-bound aggregates of antigen-antibody complexes are deposited in vessel walls or on serosal surfaces or other extravascular sites; neutrophils are chemotactically attracted and release lysosomal enzymes, prostaglandins, kinins
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| type 3 hypersensitivity | serum sickness; arthrus reaction; polyarteritis nodosa; SLE; immune complex mediated glomerular disease
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| type 4 hypersensitivity | delayed hypersensitivity; proliferation of antigen specific CD 4+ memory T cells, with secretion of IL-2 and other sytokines, which in turn recruit and stimulate phagocytosic macrophages; may also involve cytotoxic CD 8+ T lymphocyte killing of spec cells
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| hyperacute rejection | is primarily antibody-mediated and occurs in the presesnce of preexisting antibody to donor antigens
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| hperacute rejection | most often occurs within minutes; is a localized Arthrus reaction marked by acute inflammation, fibronoid necrosis of small vessels, and extensive thrombosis
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| acute rejection | primarily T cell mediated, generally occurs days to months after transplantation, characterized by infiltration of lymphocytes and macrophages
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| chronic rejection | is primarily caused by antibody-mediated vascular damage
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| chronic rejection | may occur months to years after an otherwise successful transplantation, characterized histologically by marked vascular fibroininal proliferation, often reuslting in a small, scarred kidney
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| graft-vs-host | is significant problem in bone marrow transplantation, can also be caused by whole blood transfusion in patients with SCID, characterized by rejection of foreign host cells by engurafted T and B cells
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| SLE | marked by the presence of a spectrum of ANAs and by extensive immune complex mediated inflammatory lesions
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| SLE | fever, malaise, butterfly rash, lymphadenopathy, joint symptoms,reynaud phenomenon, serosal inflammation, interstitial pulmonary fibrosis, endocarditis, glomerular changes
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