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风湿热发病机制中的自身免疫机制。

Autoimmune mechanisms in the pathogenesis of rheumatic fever.

作者信息

Senitzer D, Freimer E H

出版信息

Rev Infect Dis. 1984 Nov-Dec;6(6):832-9. doi: 10.1093/clinids/6.6.832.

DOI:10.1093/clinids/6.6.832
PMID:6084283
Abstract

The etiologic agent of acute rheumatic fever is the group A streptococcus; however, its role in the pathogenesis of this disease is not well understood. Epidemiologic and immunologic evidence suggests that there is a population at risk and that the nature of the host response to streptococcal antigens and the physicochemical nature of the streptococcal antigens all play a significant role in determining the natural history of the disease process. Furthermore, the genetic control of the interaction of the host with the streptococci is clearly involved in a set of events--as yet obscure--that result in acute rheumatic fever. Neither antibody-mediated nor cell-mediated hypersensitivity reactions have been demonstrated in vivo or in vitro that wholly reproduce the characteristics of this disease. Additional studies of the regulation of the immune response and of human immunogenetics are essential for gaining further insight into the pathogenesis of acute rheumatic fever.

摘要

急性风湿热的病原体是A组链球菌;然而,其在该疾病发病机制中的作用尚未完全明确。流行病学和免疫学证据表明,存在一个易感人群,宿主对链球菌抗原的反应性质以及链球菌抗原的物理化学性质在决定疾病进程的自然史中均起着重要作用。此外,宿主与链球菌相互作用的遗传控制显然参与了一系列尚未明确的事件,这些事件导致了急性风湿热。在体内或体外均未证实抗体介导或细胞介导的超敏反应能完全重现该疾病的特征。对免疫反应调节和人类免疫遗传学进行更多研究,对于深入了解急性风湿热的发病机制至关重要。

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TLR-2 gene Arg753Gln polymorphism is strongly associated with acute rheumatic fever in children.Toll样受体2(TLR-2)基因精氨酸753谷氨酰胺多态性与儿童急性风湿热密切相关。
J Mol Med (Berl). 2005 Jul;83(7):535-41. doi: 10.1007/s00109-005-0677-x. Epub 2005 Jun 21.
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