immuneresponse免疫應(yīng)答(文件)
【正文】 IgM first, then IgG secondary response anamnestic response, rapid, strong Role of other cells Macrophages ‘Antigen Presenting Cell’ (APC) engulf antigen。 IL5 B cell proliferates into Plasma and Memory cells Superantigens Staphylococcus enterotoxin, TSST some viruses Regular antigen – processed by macrophages epitopes on surface with MHC interact with lymphocytes with appropriate receptor Superantigen – binds directly to MHC massive lymphocyte activation (220% of all T cells) high levels of cytokines/lymphokines released Very strong immune response systemic toxicity suppression of normal immune response AntigenAntibody Reactions Toxin neutralize Soluble antigen precipitation Cells agglutination Activate: plement plement fixation activate neutrophils initiate inflammatory response lyse cell Activate phagocytosis opsonization CELLMEDIATED IMMUNITY T lymphocytes travel to site to destroy antigen subpopulations with same receptor, different function Regulatory effects: T helpers (TH) amp。 lysis Hypersensitivity Reactions Type I: anaphylaxis mediated by IgE rapid response: blood vessel dilation, hypotension, shock insect venom Type II: cytolytic/cytotoxic reactions mediated by IgG, IgM bind to cell, initiate plement cascade amp。 phagocytes attack, releasing lytic enzymes hours Type IV: delayed hypersensitivity/cell mediated reactions mediated by T cells which release lymphokines macrophage accumulation and activation begins 1824 hr, peak at 2448 hr rash of small pox, measles。 pain proteolytic enzymes of neutrophils degrade collagen repeated bouts lead to fibrous tissue replacing collagen joint fusion Hashimoto’s thyroiditis antibodies against thyroid epithelial cells amp。 cellmediated immune systems Hashimoto’s thyroiditis antibodies against thyroid epithelial cells amp。 cellmediated immune systems Multiple sclerosis ?? demyelinization of CNS tissue, progressive paralysis lesions resemble cellular infiltrates associated with delayed hypersensitivity reactions Hashimoto’s thyroiditis antibodies against thyroid epithelial cells amp。 cellmediated immune systems Multiple sclerosis ?? demyelinization of CNS tissue, progressive paralysis lesions resemble cellular infiltrates associated with delayed hypersensitivity reactions Juvenile or Type I diabetes T cells attack the ?cells of the pancreas Etiology of Autoimmune disseases Tolerance T suppressors hold system in check ‘clonal deletion’ eliminates cells able to respond to ‘self’ Autoimmunity clones not deleted hidden antigen now exposed antigens not made early now produced viral induced changes cr
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鄂ICP備17016276號-1