中文摘要：

摘要炎症小体（inflammasomes）活化后产生的IL-1β和IL-18等促炎因子对天然免疫和适应性免疫具有重要作用．炎症小体持续活化可引起促炎因子过度表达，导致慢性炎症和自身免疫疾病的发生．正常生理状态下，机体存在多种炎症小体负调机制，以维持免疫反应平衡．病理状态下，感染机体的病原微生物通过多种途径抑制炎症小体信号通路的活化及促炎因子的产生，以利于免疫逃逸．本文综述了机体和病原微生物对炎症小体信号通路的负调控机理．阐明炎症小体信号通路负调控机制将为感染性疾病及其他炎症小体相关炎症性疾病的治疗提供策略．

英文摘要：

Inflammasomes activation is critical for both innate and adaptive immunity through their regulation of interleukin 1β（IL-lβ） and IL-18. Prolonged inflammasomes activation can lead to exaggerated expression of signaling components as well as pro-inflammatory cytokines that can damage the host, resulting in chronic inflammatory diseases and autoimmune disorders. Therefore, pathways of deactivation are important to balance the immune responses. However, recent discoveries have uncovered a plethora of pathogenic strategies to inhibit the activation of inflammasome signal pathways and the production of pro-inflammatory cytokines to evade immune responses. Elucidation of these mechanisms might be helpful to the rational design of therapy against infectious diseases and other inflammasome-dependent inflammatory processes.