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婴幼儿好发的川崎病不仅在日本,在世界各地也正在增加.该病以全身性炎性病变为基础,通过伴发冠状动脉瘤引起血栓性闭塞,有时导致患儿突然死亡.关于本病的病因及发病机理目前还未被阐明.美国哈佛大学小组就本病的发病机理发表了极其简明的假说.Leung等从免疫学方面研究了川崎病的发病机理.本病免疫异常的特征是,T细胞水平:T_8±细胞(抑制性T细胞)减少及Ia±/T_4±细胞(激活的辅助性T细胞)显著增加,另外B细胞被多克隆活化.在川崎病急性期血清中有自身抗体IgM,此抗体对经Υ-干扰素处理的人脐静脉内皮细胞(HUVE)及人隐静脉内皮细胞(HSVE)有补体依赖性细胞的损害作用.晚近研究表明,对于经白细胞介
Kawasaki disease, which occurs in infants and young children, is increasing not only in Japan but also in other parts of the world. The disease is based on systemic inflammatory disease and causes thrombotic occlusion accompanied by coronary aneurysm, which may result in sudden death in children. The etiology and pathogenesis has not yet been clarified.University of Harvard team on the pathogenesis of this disease published an extremely concise hypothesis.Leung et al from the immunological aspects of the pathogenesis of Kawasaki disease.The characteristics of this disease is immune dysfunction, T cell levels: a decrease in T_8 cells (suppressor T cells) and a significant increase in Ia ± / T_4 cells (activated helper T cells), in addition to polyclonal activation of B cells In the acute phase of Kawasaki disease, there are autoantibodies IgM, this antibody on human γ-interferon-treated human umbilical vein endothelial cells (HUVE) and human saphenous vein endothelial cells (HSVE) complement-dependent cell damage.Recent studies have shown that for leukocyte mediated