《浙江大学医学免疫学经典课件免疫超敏反应》课件.pptVIP

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * Arthus’s reaction （1903） 经抗原反复免疫之后,注射抗原的皮下出现局部红肿、出血和坏死等剧烈炎症反应。 C3a C5a 肥大细胞 血小板 补体 抗体 抗原 内皮细胞 复合物 血管活性胺 C5a 中性粒细胞 血小板凝聚 免疫复合物沉淀 趋化 活性酶 微血栓形成 基底膜 血管壁 1 2 2. Serum sickness Serum sickness is a complication of serum therapy, in which massive doses of anti-serum are given in conditions such as snake bite. Serum sickness（血清病） Clemens Pirquet 1874-1929 3. Postinfectious glomerulonephritis 常见于A族溶血性链球菌感染后2-3周。抗体与链球菌可溶性抗原形成复和物，沉积于肾小球基底膜处 Human immune complex disease 4. Rheumatoid arthritis Rheumatoid factor (RF): an immunoglobulin (mainly IgM but also IgG and IgA) with antibody specificity for the Fc portion of IgG. The joint synovial fluid contains IC consisting of RF-IgG-complement. Many patients with rheumatoid arthritis also have antinuclear antibodies. 5. Systemic lupus erythematosus (SLE) antinuclear antibodies hypergammaglobulinemia 自身抗体与可溶性自身抗原形成免疫复和物，沉积于皮下、关节和肾小球基底膜等处。 RA，SLE SLE Type IV hypersensitivity(Delayed type hypersensitivity) Delayed type hypersensitivity is initiated by sensitized T cells reacting with specific antigens. The reactions are manifest as inflammation at the site of antigen exposure, which usually peaks 24-72 hours after exposure. This reaction is independent of antibody and complement. I. Pathogenic mechanisms Ag-MHC Antigen→APC→T cells co-stimulating factors↓ sensitized T cell ↓ effector and memory cells ↓ ↓ CD4+T cell (Th1 type) CD8+T cell (CTL) ↓ ↓ release of cytokines killing target cells ↓ by the release of inducing the inflammatory perforin and granzymes response