Inflammation, a vital response of the immune system to infection and damage to tissues, can be initiated by various germline-encoded innate immune-signaling receptors. Among these, the inflammasomes are critical for activation of the potent proinflammatory interleukin-1 cytokine family. Additionally, inflammasomes can trigger and maintain inflammatory responses aimed toward excess nutrients and the numerous danger signals that appear in a variety of chronic inflammatory diseases. We discuss our understanding of how inflammasomes assemble to trigger caspase-1 activation and subsequent cytokine release, describe how genetic mutations in inflammasome-related genes lead to autoinflammatory syndromes, and review the contribution of inflammasome activation to various pathologies arising from metabolic dysfunction. Insights into the mechanisms that govern inflammasome activation will help in the development of novel therapeutic strategies, not only for managing genetic diseases associated with overactive inflammasomes, but also for treating common metabolic diseases for which effective therapies are currently lacking.

中文翻译：

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炎症小体和自身炎症综合症。

炎症是免疫系统对感染和组织损伤的重要反应，它可以由多种种系编码的先天免疫信号受体引发。其中，炎症小体对于激活有效的促炎性白介素-1细胞因子家族至关重要。另外，炎症小体可以触发和维持针对过多营养物的炎症反应，以及各种慢性炎症疾病中出现的众多危险信号。我们讨论了我们对炎症小体如何组装以触发caspase-1激活和随后的细胞因子释放的理解，描述了炎症小体相关基因的基因突变如何导致自身炎症综合症，并回顾了炎症小体激活对代谢功能异常引起的各种病理的贡献。