NLRP3炎症小体在自身免疫性肝炎中的作用机制

Research advances in the mechanism of action of nucleotide-binding oligomerization domain-like receptor protein 3 inflammasome in autoimmune hepatitis

自身免疫性肝炎(AIH)是由自身免疫系统攻击肝细胞所致的慢性肝炎,目前关于AIH的发病机制尚不十分明确。炎症小体是先天免疫的重要组成部分,参与多种病理生理学过程。研究表明核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎性小体相关的炎性反应在AIH的发病机制中起重要作用,其主要介导促炎因子的释放和细胞焦亡,进而参与AIH的病理生理过程。因此,可以通过抑制NLRP3炎性小体的激活来延缓AIH发生发展,从而为AIH的防治提供新思路。

Autoimmune hepatitis(AIH)is chronic hepatitis caused by the attack of live cells by the immune system,and at present,the pathogenesis of AIH remains unclear.Inflammasomes are important components of innate immunity and are involved in a variety of pathophysiological processes.Studies have shown that inflammatory response associated with nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)plays an important role in the pathogenesis of AIH,which mainly mediates the release of proinflammatory factors and pyroptosis,thereby participating in the pathophysiological process of AIH.Therefore,the development and progression of AIH can be delayed by inhibiting the activation of NLRP3 inflammasomes,which provides new ideas for the prevention and treatment of AIH.