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首页> 外文期刊>Frontiers in bioscience: a journal and virtual library >DP IV/CD26, APN/CD13 and related enzymes as regulators of T cell immunity: implications for experimental encephalomyelitis and multiple sclerosis.
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DP IV/CD26, APN/CD13 and related enzymes as regulators of T cell immunity: implications for experimental encephalomyelitis and multiple sclerosis.

机译：DP IV / CD26，APN / CD13和相关酶作为T细胞免疫的调节剂：对实验性脑脊髓炎和多发性硬化症的影响。

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摘要

Multiple sclerosis (MS) is the most frequent demyelinating disease of the central nervous system. Peptidases like dipeptidyl peptidase IV (DP IV, CD26) and aminopeptidase N (APN, CD13) play a regulatory role in T cell activation and represent potential targets for the treatment of inflammatory disorders. Synthetic inhibitors of DP IV and/or APN enzymatic activity induce production of the immunosuppressive cytokine TGF-beta1 and subsequently suppress DNA synthesis and Th1 cytokine production of activated human T cells. Compelling evidence has demonstrated that IL-17-producing CD4 cells (Th17) are a major contributor to the pathogenesis of autoimmune inflammation. Here, we report that inhibitors of DP IV-like activity as well as of APN activity inhibit IL-17 production in activated human and mouse T cells. Combining inhibitors of DP IV and APN increases the suppressive effect on T cell specific IL-17 production in vitro compared to a single peptidase inhibitor. In the following, we summarize the evidence for the role of both ectoenzymes in T cell activation in vitro and in vivo and provide a rationale for the use of combined or dual ectopeptidase inhibitors to treat autoimmune diseases like MS.
机译：多发性硬化症（MS）是中枢神经系统最常见的脱髓鞘疾病。像二肽基肽酶IV（DP IV，CD26）和氨基肽酶N（APN，CD13）之类的肽酶在T细胞活化中起调节作用，并代表了治疗炎症性疾病的潜在靶标。 DP IV和/或APN酶活性的合成抑制剂诱导免疫抑制细胞因子TGF-beta1的产生，并随后抑制活化的人T细胞的DNA合成和Th1细胞因子的产生。有力的证据表明，产生IL-17的CD4细胞（Th17）是自身免疫炎症发病机理的主要贡献者。在这里，我们报告说，DP IV样活性以及APN活性的抑制剂在激活的人和小鼠T细胞中抑制IL-17的产生。与单一肽酶抑制剂相比，DP IV和APN抑制剂的组合在体外增加了对T细胞特异性IL-17产生的抑制作用。在下文中，我们总结了体外和体内两种外切酶在T细胞活化中的作用的证据，并为使用联合或双重表位肽酶抑制剂治疗自身免疫性疾病（如MS）提供了理论依据。

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