【摘要】 银屑病是一种慢性自身免疫性炎症性皮肤病,其发病机制目前尚未完全阐明。黑色素瘤缺乏因子2(AIM2)是一种参与天然免疫的感受器,可识别双链脱氧核糖核酸(dsDNA)并进一步组装成为AIM2炎症小体。AIM2炎症小体是一种蛋白质复合体,然而AIM2对胞质自身脱氧核糖核酸(DNA)的不正确识别可导致银屑病、特应性皮炎、关节炎等自身免疫性和炎症性疾病的发生与发展,故抑制AIM2炎症小体激活有望成为银屑病的治疗新靶点。现将AIM2在银屑病中的作用机制和实验模型中AIM2炎症小体在银屑病中作用的证据综述如下。更多还原

【Abstract】 Psoriasis is chronic autoimmune inflammatory skin disease and its pathogenesis has not been fully understood. Absent in melanoma 2(AIM2) is a sensor involved in innate immune response,can recognize double stranded deoxyribonucleic acid(ds DNA) and further assemble them into AIM2 inflammosome. AIM2 inflammasome is a protein complex,while inappropriate recognition of cytoplasmic self-DNA by AIM2 contributes to the development of psoriasis,atopic dermatitis,arthritis and other autoimmune as well as inflammatory diseases. Therefore,inhibition of AIM2 inflammasome activation is expected to be a new therapeutic target for psoriasis. This article reviewed the mechanism of AIM2 in psoriasis and the evidence of AIM2 inflammasome involving in the pathogenesis of experimental psoriasis model.更多还原