炎性小体:一个调节免疫反应和疾病发病机制的半胱天冬酶-1激活平台。

The inflammasome: a caspase-1-activation platform that regulates immune responses and disease pathogenesis.

作者信息

Franchi Luigi, Eigenbrod Tatjana, Muñoz-Planillo Raúl, Nuñez Gabriel

机构信息

Department of Pathology, Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, Michigan 48109, USA.

出版信息

Nat Immunol. 2009 Mar;10(3):241-7. doi: 10.1038/ni.1703.

Abstract

The inflammasome is a multiprotein complex that mediates the activation of caspase-1, which promotes secretion of the proinflammatory cytokines interleukin 1beta (IL-1beta) and IL-18, as well as 'pyroptosis', a form of cell death induced by bacterial pathogens. Members of the Nod-like receptor family, including NLRP1, NLRP3 and NLRC4, and the adaptor ASC are critical components of the inflammasome that link microbial and endogenous 'danger' signals to caspase-1 activation. Several diseases are associated with dysregulated activation of caspase-1 and secretion of IL-1beta. Thus, understanding inflammasome pathways may provide insight into disease pathogenesis that might identify potential targets for therapeutic intervention.

摘要

炎性小体是一种多蛋白复合物,介导半胱天冬酶 -1的激活,半胱天冬酶 -1可促进促炎细胞因子白细胞介素 1β(IL-1β)和 IL-18的分泌,以及“细胞焦亡”,这是一种由细菌病原体诱导的细胞死亡形式。Nod样受体家族的成员,包括 NLRP1、NLRP3和 NLRC4,以及接头蛋白 ASC是炎性小体的关键组成部分,它们将微生物和内源性“危险”信号与半胱天冬酶 -1的激活联系起来。几种疾病与半胱天冬酶 -1的失调激活和 IL-1β的分泌有关。因此,了解炎性小体途径可能有助于深入了解疾病发病机制,从而确定潜在的治疗干预靶点。

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