炎性小体信号的负向调控

Pub Date : 2014-01-01 DOI:10.3724/SP.J.1206.2013.00306
Z. Cai, Y. Xin
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引用次数: 0

摘要

炎性小体的激活通过调节白细胞介素1β(IL-1β)和IL-18对先天免疫和适应性免疫至关重要。炎症小体的长期激活可导致信号成分和促炎细胞因子的过度表达,从而损害宿主,导致慢性炎症性疾病和自身免疫性疾病。因此,失活途径对于平衡免疫反应是重要的。然而,最近的发现发现了大量的致病策略来抑制炎症小体信号通路的激活和促炎细胞因子的产生,以逃避免疫反应。阐明这些机制可能有助于合理设计针对传染病和其他炎性小体依赖性炎症过程的治疗方法。
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Negative Regulation of Inflammasome Signaling
Inflammasomes activation is critical for both innate and adaptive immunity through their regulation of interleukin 1β(IL-1β) 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.
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