角质形成细胞与T细胞的crosstalk诱发银屑病的研究现状及展望  

The crosstalk between keratinocytes and T cells in the pathogenesis of psoriasis

作　　者：吴叶林[1] 全艳春[1] 赖玉平[1] 

机构地区：[1]华东师范大学生命科学学院上海市调控生物学重点实验室,上海200241

出　　处：《生命科学》2016年第2期258-267,共10页Chinese Bulletin of Life Sciences

基　　金：国家自然科学基金项目(31222021;31470878;31170867;81202327);教育部新世纪优秀人才项目(NCET-11-0141);上海市科委项目(13JC1402301);上海市教委项目(13SG25);霍英东教育基金会项目(141017)

摘　　要：银屑病作为一种常见的慢性炎症性皮肤病,其在皮肤上的主要特征表现为角质形成细胞过度增殖并伴有炎性细胞浸润。虽然已知T细胞通过分泌大量的细胞因子,如IL-17、TNF-α等能诱发银屑病,但对于角质形成细胞如何影响T细胞的活化导致皮肤炎症级联放大而恶化银屑病病程仍知之甚少。近年来,绝大多数的研究集中在证明IL-23/IL-17/IL-22轴是银屑病中皮肤炎性细胞浸润和表皮层增生的主要诱因。这些研究将角质形成细胞作为银屑病病发的一个readout,而忽略了角质形成细胞对T细胞分化和活化的影响在银屑病致病过程中的重要作用以及角质形成细胞、树突状细胞和T细胞之间错综复杂的相互作用。因此,这篇综述将总结角质形成细胞和T细胞在银屑病发生、发展中所起的重要作用,尤其是角质形成细胞、树突状细胞与T细胞相互调节、相互制约的网络调控体系在银屑病致病过程中的决定作用,从而为临床更好地诊治银屑病提供理论指导。Psoriasis is a chronic inflammatory disease accompanied by keratinocyte hyperproliferation andleukocyte infiltration. Although it is known that cytokines such as IL-17 and TNF-α from T cells are strongly linked with psoriasis, how keratinocytes affect the differentiation and expansion of T cells and induce a positive feedforward mechanism to amplify local inflammatory responses is not fully understood. Accumulating evidence demonstrates that IL-23/IL-17/IL-22 axis plays a crucial role in leukocyte recruitment and epidermal hyperproliferation. In these studies keratinocytes are thought to act as the readout in the pathogenesis of psoriasis, while the influence of keratinocytes on T cell differentiation and expansion and the important role of crosstalk among keratinocytes, dendritic cells and T cells in the pathogenesis of psoriasis are neglected. Here we summarize how keratinocytes and T cells play roles in the pathogenesis of psoriasis, especially how keratinocytes, dendritic cells and T cells form a network to control the development of psoriasis, and provide new insights into the treatment of psoriasis.

关 键 词：银屑病 角质形成细胞 T细胞 树突状细胞 CROSSTALK 

分 类 号：R392[医药卫生—免疫学] R758.63[医药卫生—基础医学]