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首页> 外文期刊>Journal of Autoimmunity >Chemokine receptor CXCR3 deficiency exacerbates murine autoimmune cholangitis by promoting pathogenic CD8(+) T cell activation
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Chemokine receptor CXCR3 deficiency exacerbates murine autoimmune cholangitis by promoting pathogenic CD8(+) T cell activation

机译：趋化因子受体CXCR3缺乏通过促进致病CD8（+）T细胞活化来加剧鼠自身免疫性胆管炎

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CXC Chemokine Receptor 3 (CXCR3) is functionally pleiotropic and not only plays an important role in chemotaxis, but also participates in T cell differentiation and may play a critical role in inducing and maintaining immune tolerance. These observations are particularly critical for autoimmune cholangitis in which CXCR3 positive T cells are found around the portal areas of both humans and mouse models of primary biliary cholangitis (PBC). Herein, we investigated the role of CXCR3 in the pathogenesis of autoimmune cholangitis. We have taken advantage of a unique CXCR3 knockout dnTGF beta RII mouse to focus on the role of CXCR3, both by direct observation of its influence on the natural course of disease, as well as through adoptive transfer studies into Rag -/- mice. We report herein that not only do CXCR3 deficient mice develop an exacerbation of autoimmune cholangitis associated with an expanded effector memory T cell number, but also selective adoptive transfer of CXCR3 deficient CD8(+) T cells induces autoimmune cholangitis. In addition, gene microarray analysis of CXCR3 deficient CD8(+) T cells reveal an intense pro-inflammatory profile. Our data suggests that the altered gene profiles induced by CXCR3 deficiency promotes autoimmune cholangitis through pathogenic CD8(+) T cells. These data have significance for human PBC and other autoimmune liver diseases in which therapeutic intervention might be directed to chemokines and/or their receptors. (C) 2017 Elsevier Ltd. All rights reserved.
机译：CXC趋化因子受体3（CXCR3）在功能性肺炎中，不仅在趋化性中起重要作用，而且还参与T细胞分化，并且可能在诱导和维持免疫耐受中发挥关键作用。这些观察结果对于自身免疫性胆管炎特别关键，其中CXCR3阳性T细胞在原发性胆管炎（PBC）两种人和小鼠模型的门户网站上发现。在此，我们研究了CXCR3在自身免疫性胆管炎的发病机制中的作用。我们利用了独特的CXCR3淘汰赛DNTGF Beta RII鼠标，专注于CXCR3的作用，通过直接观察其对自然疾病进程的影响，以及通过养老金 - / - 小鼠的养殖研究。我们报告的是，CXCR3缺陷小鼠不仅会产生与膨胀效应记忆T细胞数相关的自身免疫性胆管炎的恶化，而且还具有CXCR3缺陷CD8（+）T细胞的选择性接受转移诱导自身免疫性胆管炎。此外，CXCR3缺陷CD8（+）T细胞的基因微阵列分析显示出浓度的促炎症。我们的数据表明，CXCR3缺乏诱导的改变的基因谱通过致病CD8（+）T细胞促进了自身免疫性胆管炎。这些数据对人PBC和其他自身免疫肝病具有重要意义，其中治疗干预可能针对趋化因子和/或其受体。 （c）2017 Elsevier Ltd.保留所有权利。

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