Negative Regulation of Inflammasome Signaling

Abstract

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.