银屑病基因-基因交互作用研究进展

全基因组关联研究发现，对基因-基因交互作用在银屑病发病中的研究取得了积极进展，增进了对银屑病遗传学发病机制的认识。目前，银屑病基因-基因交互作用主要集中在主要组织相容性复合体易感区域和IL23／Thl7信号通路。主要组织相容性复合体区域是最早被发现而且是银屑病发病机制中最重要的易感区域。研究表明，其与内质网氨基肽酶1（ERAPl）基因、抑半胱氨酸蛋白酶蛋白A（CSTA）基因、LCE基因簇及染色体19p13区域（PSORS6）等存在相互作用。白介素23／Thl7是一个与慢性炎症性疾病发病密切相关的重要通路，研究发现其中的多个基因在银屑病发病中存在交互作用。

Gene-gene interactions in psoriasis

In recent years, significant breakthroughs have been made in the search for psoriasis susceptibility genes through genome-wide association studies （GWAS）, and positive evidences have also been established for gene-gene interactions in the pathogenesis of psoriasis, both of which greatly increase the understanding of psoriasis pathogenesis. Moreover, these interactions mainly occur in the major histocompatibility complex （MHC） region and interleukin-23 （IL-23）/T helper 17 （Thl7） pathway. The MHC region, the first susceptible region identified for psoriasis, is thought to be the most important region in the pathogenesis of psoriasis. Evidences have been found for the interactions between HLA-Cw6 and various genes including the endoplasmic reticulum aminopeptidase 1 （ERAP1） gene, cystatin A （CSTA） gene, LCE gene cluster, chromosome 19p13 region （PSORS6）, etc. The IL-23/Th17 pathway is closely associated with the pathogenesis of several chronic inflammatory diseases, and muhiple genes in this pathway are found to interact mutually in the initiation of psoriasis.