炎症小体是高分子量的蛋白质复合物,可以裂解两种主要的促炎细胞因子,前白细胞介素-1β和前白细胞介素-18,活性形式,并有助于牛皮癣。尽管最近在银屑病的发病机制方面取得了进展,主要研究为自身免疫性疾病,激活免疫反应触发牛皮癣仍未完全了解。最近,重点放在炎症小体在银屑病发病机制中的作用。多种类型的各种炎性体的抑制剂和活化剂,炎症相关基因,和遗传易感位点在银屑病中被识别。在这次系统性审查中,我们从炎性体中收集了最近的全面证据,NLRP1、NLRP3和AIM2在银屑病发病中的作用.
Inflammasomes are high-molecular-weight protein complexes that may cleave the two main proinflammatory cytokines, pro-interleukin-1β and pro-interleukin-18, into active forms, and contribute to psoriasis. Despite recent advances made in the pathogenesis of psoriasis, mainly studied as an autoimmune condition, activation of immune response triggers of psoriasis is still not completely understood. Recently, focus was placed on the role of inflammasomes in the pathogenesis of psoriasis. Multiple types of inhibitors and activators of various inflammasomes, inflammasome-related genes, and genetic susceptibility loci were recognized in psoriasis. In this systemic
review, we collect recent and comprehensive evidence from the inflammasomes,
NLRP1, NLRP3, and AIM2, in pathogenesis of psoriasis.