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复发性外阴阴道念珠菌病的免疫发病机制。

Immunopathogenesis of recurrent vulvovaginal candidiasis.

作者信息

Fidel P L, Sobel J D

机构信息

Division of Infectious Diseases, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

出版信息

Clin Microbiol Rev. 1996 Jul;9(3):335-48. doi: 10.1128/CMR.9.3.335.

Abstract

Recurrent vulvovaginal candidiasis (RVVC) is a prevalent opportunistic mucosal infection, caused predominantly by Candida albicans, which affects a significant number of otherwise healthy women of childbearing age. Since there are no known exogenous predisposing factors to explain the incidence of symptomatic vaginitis in most women with idiopathic RVVC, it has been postulated that these particular women suffer from an immunological abnormality that prediposes them to RVVC. Because of the increased incidence of mucosal candidiasis in individuals with depressed cell-mediated immunity (CMI), defects in CMI are viewed as a possible explanation for RVVC. In this review, we attempt to place into perspective the accumulated information regarding the immunopathogenesis of RVVC, as well as to provide new immunological perspectives and hypotheses regarding potential immunological deficiencies that may predispose to RVVC and potentially other mucosal infections by the same organism. The results of both clinical studies and studies in an animal model of experimental vaginitis suggest that systemic CMI may not be the predominant host defense mechanism against C. albicans vaginal infections. Rather, locally acquired mucosal immunity, distinct from that in the peripheral circulation, is now under consideration as an important host defense at the vaginal mucosa, as well as the notion that changes in local CMI mechanism(s) may predispose to RVVC.

摘要

复发性外阴阴道念珠菌病(RVVC)是一种常见的机会性黏膜感染,主要由白色念珠菌引起,影响大量其他方面健康的育龄妇女。由于在大多数特发性RVVC女性患者中,尚无已知的外源性诱发因素可解释症状性阴道炎的发病率,因此据推测,这些特定女性存在免疫异常,使她们易患RVVC。由于细胞介导免疫(CMI)低下的个体黏膜念珠菌病发病率增加,CMI缺陷被视为RVVC的一种可能解释。在本综述中,我们试图正确看待有关RVVC免疫发病机制的累积信息,并就可能使个体易患RVVC以及可能易患同一病原体引起的其他黏膜感染的潜在免疫缺陷提供新的免疫学观点和假设。临床研究以及实验性阴道炎动物模型研究的结果表明,全身性CMI可能不是抵御白色念珠菌阴道感染的主要宿主防御机制。相反,与外周循环不同的局部获得性黏膜免疫,目前被认为是阴道黏膜重要的宿主防御机制,以及局部CMI机制的变化可能使个体易患RVVC这一观点。

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