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共刺激分子在银屑病中的作用及其对靶向治疗的意义。

The Role of Co-Signaling Molecules in Psoriasis and Their Implications for Targeted Treatment.

作者信息

Liu Suqing, Xu Jinhua, Wu Jinfeng

机构信息

Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

出版信息

Front Pharmacol. 2021 Jul 20;12:717042. doi: 10.3389/fphar.2021.717042. eCollection 2021.

Abstract

Psoriasis is a chronic, systemic immune-mediated inflammatory disease manifesting in the skin, joint or both. Co-signaling molecules are essential for determining the magnitude of the T cell response to the antigen. According to the function of co-signaling molecules, they can be divided into co-stimulatory molecules and co-inhibitory molecules. The role of co-signaling molecules in psoriasis is recognized, mainly including the co-stimulatory molecules CD28, CD40, OX40, CD27, DR3, LFA-1, and LFA-3 and the co-inhibitory molecules CTLA-4, PD-1, and TIM-3. They impact the pathological process of psoriasis by modulating the immune strength of T cells, regulating the production of cytokines or the differentiation of Tregs. In recent years, immunotherapies targeting co-signaling molecules have made significant progress and shown broad application prospects in psoriasis. This review aims to outline the possible role of co-signaling molecules in the pathogenesis of psoriasis and their potential application for the treatment of psoriasis.

摘要

银屑病是一种慢性、全身性免疫介导的炎症性疾病,可表现在皮肤、关节或两者皆有。共信号分子对于确定T细胞对抗原的反应强度至关重要。根据共信号分子的功能,它们可分为共刺激分子和共抑制分子。共信号分子在银屑病中的作用已得到认可,主要包括共刺激分子CD28、CD40、OX40、CD27、DR3、淋巴细胞功能相关抗原-1(LFA-1)和淋巴细胞功能相关抗原-3(LFA-3)以及共抑制分子细胞毒性T淋巴细胞相关蛋白4(CTLA-4)、程序性死亡受体1(PD-1)和T细胞免疫球蛋白黏蛋白分子3(TIM-3)。它们通过调节T细胞的免疫强度、调节细胞因子的产生或调节性T细胞(Tregs)的分化来影响银屑病的病理过程。近年来,针对共信号分子的免疫疗法取得了重大进展,并在银屑病治疗中显示出广阔的应用前景。本综述旨在概述共信号分子在银屑病发病机制中的可能作用及其在银屑病治疗中的潜在应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1e0/8329336/6afd3e30e4e2/fphar-12-717042-g001.jpg

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