莱姆病(莱姆病):伯氏疏螺旋体与人类(和其他哺乳动物)宿主的相互作用

L.H. Sigal
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引用次数: 2

摘要

20年来,莱姆病已经从康涅狄格河东岸三个小社区的新奇事物发展成为美国和德国最常见的媒介传播疾病,并引起了全世界的关注。在这么短的时间内,病原学病原体已被识别和发展,由该病原体引起的临床综合征已被描述,血清确认试验已被开发,有效的治疗方案已确定,疫苗已被发现安全有效,流行病学和生态学已被充分了解以建立避免和预防策略。然而,病原病原体伯氏疏螺旋体(Borrelia burgdorferi sensu lato)实际导致组织损伤/功能障碍的机制仍有待确定。以下是对一些提出的免疫致病机制的综述,重点是可能的自身免疫。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lyme borreliosis (Lyme disease): interactions of Borrelia burgdorferi sensu lato with human (and other mammalian) hosts

In the twenty years since its description, Lyme disease has evolved from being a curiosity in three small communities on the east bank of the Connecticut River to the most common vector-borne disease in the U.S. and Germany, and a worldwide concern. In this short time, the aetiologic agent has been identified and grown, the clinical syndromes due to this agent have been delineated, seroconfirmatory tests developed, effective therapeutic regimens determined, a vaccine found safe and effective, and the epidemiology and ecology understood sufficiently to establish avoidance and prevention strategies. However, the mechanisms whereby the aetiologic agent, Borrelia burgdorferi sensu lato actually causes tissue damage/dysfunction remain to be defined. The following represents a review of some proposed immunopathogenic mechanisms with a focus on possible autoimmunity.

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