Institute for Clinical Chemistry and Clinical Pharmacology, Unit for Clinical Biochemistry, University Hospital, University of Bonn, Bonn, Germany.
Clin Exp Immunol. 2012 Mar;167(3):369-81. doi: 10.1111/j.1365-2249.2011.04534.x.
OTHER THEMES PUBLISHED IN THIS IMMUNOLOGY IN THE CLINIC REVIEW SERIES Allergy, Host Responses, Cancer, Type 1 diabetes and viruses, Metabolic diseases.
Initiation of a successful immune response requires a working set of sensors that detect any noxious agent within the cellular microenvironment and molecular platforms that process this signal to trigger an appropriate effector response. Pattern recognition receptors can engage different signalling cascades that lead to proinflammatory gene expression. At the same time, transcription-independent events such as activation of proteases and/or phagocytosis are also initiated. The inflammasome pathway constitutes a signalling platform that leads to the activation of so-called inflammatory caspases, most notably caspase-1, which plays a pivotal role in the cleavage and thus maturation of proinflammatory cytokines, but also in the induction of pyroptosis, a special type of cell death. In this review we elaborate on the currently known inflammasome complexes with a special focus on the mechanism behind their activation. Understanding these mechanisms could provide important information regarding the potential signalling nodes that might be targeted for therapeutic intervention.
本免疫学临床评论系列中的其他主题包括过敏、宿主反应、癌症、1 型糖尿病和病毒、代谢疾病。
成功的免疫反应的启动需要一组工作传感器，这些传感器可以检测细胞微环境中的任何有害物质，以及处理该信号以触发适当效应器反应的分子平台。模式识别受体可以参与不同的信号级联，导致促炎基因的表达。与此同时，也会启动转录非依赖性事件，如蛋白酶的激活和/或吞噬作用。炎性小体途径构成了一个信号平台，导致所谓的炎性半胱天冬酶的激活，特别是半胱天冬酶-1，它在促炎细胞因子的切割和成熟中起着关键作用，但也在细胞焦亡的诱导中起着关键作用，细胞焦亡是一种特殊类型的细胞死亡。在这篇综述中，我们详细阐述了目前已知的炎性小体复合物，特别关注它们激活的机制。了解这些机制可以为可能的信号节点提供重要信息，这些信号节点可能是治疗干预的目标。
