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宿主对原生动物寄生虫反应中的炎性小体。

Inflammasomes in host response to protozoan parasites.

作者信息

Zamboni Dario S, Lima-Junior Djalma S

机构信息

Department of Cell Biology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.

出版信息

Immunol Rev. 2015 May;265(1):156-71. doi: 10.1111/imr.12291.

Abstract

Inflammasomes are multimeric complexes of proteins that are assembled in the host cell cytoplasm in response to specific stress signals or contamination of the cytoplasm by microbial molecules. The canonical inflammasomes are composed of at least three main components: an inflammatory caspase (caspase-1, caspase-11), an adapter molecule (such as ASC), and a sensor protein (such as NLRP1, NLRP3, NLRP12, NAIP1, NAIP2, NAIP5, or AIM2). The sensor molecule determines the inflammasome specificity by detecting specific microbial products or cell stress signals. Upon activation, these molecular platforms facilitate restriction of microbial replication and trigger an inflammatory form of cell death called pyroptosis, thus accounting for the genesis of inflammatory processes. Inflammasome activation has been widely reported in response to pathogenic bacteria. However, recent reports have highlighted the important role of the inflammasomes in the host response to the pathogenesis of infections caused by intracellular protozoan parasites. Herein, we review the activation and specific roles of inflammasomes in recognition and host responses to intracellular protozoan parasites such as Trypanosoma cruzi, Toxoplasma gondii, Plasmodium spp., and Leishmania spp.

摘要

炎性小体是蛋白质的多聚体复合物,在宿主细胞质中响应特定应激信号或微生物分子污染而组装。典型的炎性小体至少由三个主要成分组成:炎性半胱天冬酶(半胱天冬酶-1、半胱天冬酶-11)、衔接分子(如ASC)和传感蛋白(如NLRP1、NLRP3、NLRP12、NAIP1、NAIP2、NAIP5或AIM2)。传感分子通过检测特定的微生物产物或细胞应激信号来决定炎性小体的特异性。激活后,这些分子平台促进对微生物复制的限制,并引发一种称为细胞焦亡的炎性细胞死亡形式,从而解释了炎症过程的发生。炎性小体激活在对病原菌的反应中已被广泛报道。然而,最近的报道强调了炎性小体在宿主对细胞内原生动物寄生虫引起的感染发病机制反应中的重要作用。在此,我们综述炎性小体在识别和宿主对细胞内原生动物寄生虫(如克氏锥虫、刚地弓形虫、疟原虫属和利什曼原虫属)反应中的激活及特定作用。

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