[基础医学]hypersensitivity-2.ppt

Hypersensitivity-II Type II hypersensitivity 由IgG或IgM类抗体与靶细胞表面抗原结合后，在补体、吞噬细胞和NK细胞参与下，引起的以细胞溶解或组织损伤为主的病理性免疫反应 II型超敏反应的损伤机制 Features： Ag is on surface of self-cell Ab is IgG or IgM Complements , macrophage ,NK cells participated in cell lysis or tissue injury 新生儿溶血的预防 3.药物过敏性溶血性贫血 Drug-induced hemolytic anemia Drugs such as aspirin and antibiotics can bind to the antigen on the surfaces of RBC. These interactions act similar to hapten-carrier conj. Such complexes can trigger Ab-mediated cell lysis by complement activation or opsonization Production of anti-penicillin antibodies 病因：溶血性链球菌感染（异嗜性抗原） 临床特点: 以肺出血和进行性肾功能衰竭为特征 发生机制: 5.自身免疫性受体病 Grave’s disease Myasthenia gravis （甲状腺功能亢进） （重症肌无力） Type III hypersensitivity ——immune complex disease Features Ig G or IgM participate in Type III hypersensitivity Immune complex persist and eventually deposit in a range of tissues and organs. The complement and effector cell mediated tissue damage. 免疫复合物的形成和沉积的影响因素 免疫复合物沉积的影响因素 机体清除免疫复合物的能力 吞噬细胞的功能缺陷 先天性补体缺陷 解剖和血流动力学因素 易沉积在肾小球、滑膜部位 炎症介质的作用 3.血小板的作用： 临床常见的III型超敏反应性疾病 局部免疫复合物病 全身性免疫复合物病/循环免疫复合物病 The diseases caused by Type III hypersensitivity Arthus reaction（Arthus 反应） Mechanism of Arthus reaction 血清病 Rheumatoid arthritis（风湿性关节炎） 自身抗体与可溶性自身抗原形成免疫复和物，沉积于关节滑膜处 Poststreptococcal glomerulonephritis (免疫复和物型肾小球肾炎) Type IV: Delayed type hypersensitivity (DTH ）——迟发型超敏反应 a hypersensitivity reaction mediated by antigen-specific effector T cells (Th1) delayed reaction: arises in 24~72 hours after encounter with the same antigen pathological change is an inflammation characterized by infiltration of macrophage and lymphocyte No antibody and complement attend The antigen that induce DTH Pathogenesis of DTH Granuloma （肉芽肿） 肉芽肿是临床