内质网氨基肽酶1在银屑病发病中的作用

银屑病是一种慢性炎症性皮肤病，其发病机制尚不清楚，可能涉及遗传、环境及自身免疫等多方面因素。近年来，随着全基因组关联研究的进展，众多银屑病易感位点陆续被发现，内质网氨基肽酶1基因便是其中之一。几乎所有种族人群的研究均表明，内质网氨基肽酶1区域的许多单核苷酸多肽性与银屑病相关，且与HLA—c之间可能存在交互作用。内质网氨基肽酶1参与人白细胞抗原I类分子翻译后的加工，并与多种细胞膜表面受体的分裂有关。内质网氨基肽酶1还参与免疫调节，尤其与cD8T细胞的活化有关，与其他炎性细胞和细胞因子共同作用，诱发或维持银屑病的皮损。

Roles of endoplasmic reticulum aminopeptidase-1 in the pathogenesis of psoriasis

Psoriasis is a chronic inflammatory skin disease. The pathogenesis of psoriasis remains unclear, and is considered to he associated with genetics, environment and autoimmunity. In recent years, with the progress in genome-wide association studies, numerous susceptibility loci have been successively identified for psoriasis, including the endoplasmic reticulum aminopeptidase-1 （ERAP1） gene. A lot of single nueleotide polymorphisms （SNPs） inside the ERAP1 gene have been repeatedly confirmed to be associated powerfully with psoriasis in nearly all ethnic/racial populations, and there might be some interactions between ERAP1 and HLA-C. ERAP1 is also involved in the trimming of HLA class I molecules to an optimal length and in the cleavage of several cytokine cell surface receptors. Moreover, ERAP1 takes part in immune regulation, in particular the activation of CD8＋ T cells, and plays a certain role in the induction and maintenance of psoriatic lesions via cooperating with other inflammatory cells and cytokines.