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autoimmunity

pathology of autoimmune disease

QuestionAnswer
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
IL-1 from monocytes, macrophages; stimulates T cell proliferation and IL-2 production
IL-2 macrophages, T cells and NK cells; stimulates proliferation of T cells, B cells, and NK cells; activates monocytes
IL-3 T cells; acts as growth factor for tissue mast cells and hematopoietic stem cells
IL-4 T cells; promotes growth of B cells and T cells; enhances expression of HLA class II antigens
IL-5 T cells; promotes end stage maturation of B cells into plasma cells
IL-6 T cells, monocytes; promotes maturation of B and T cells; inhibits growth of fibroblasts
IFN ALpha B cells and macrophages; has antiviral activity
IFN beta fibroblasts; has antiviral activity
IFN gamma T cells and NK cells; has antiviral activity; activates macrophages; enhances expression of HLA class II antigens
TNF alpha macrophages, T cells, and NK cells; stimulates T cell proliferation and IL-2 production; cytotoxic to some tumor cells
TNF beta T cells; stimulates T cell proliferation and IL-2 production; cytotoxic to some tumor cells
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
Type 1 hypersensitivity hay fever; allergic asthma; hives; anaphylactic shock
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
type 2 hypersensitivity warm antibody autoimmune hemolytic anemia;hemolytic disease of the newborn; goodpasture syndrome; graves disease
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
type 3 hypersensitivity serum sickness; arthrus reaction; polyarteritis nodosa; SLE; immune complex mediated glomerular disease
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
hyperacute rejection is primarily antibody-mediated and occurs in the presesnce of preexisting antibody to donor antigens
hperacute rejection most often occurs within minutes; is a localized Arthrus reaction marked by acute inflammation, fibronoid necrosis of small vessels, and extensive thrombosis
acute rejection primarily T cell mediated, generally occurs days to months after transplantation, characterized by infiltration of lymphocytes and macrophages
chronic rejection is primarily caused by antibody-mediated vascular damage
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
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
SLE marked by the presence of a spectrum of ANAs and by extensive immune complex mediated inflammatory lesions
SLE fever, malaise, butterfly rash, lymphadenopathy, joint symptoms,reynaud phenomenon, serosal inflammation, interstitial pulmonary fibrosis, endocarditis, glomerular changes
Created by: swohlers
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