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溃疡性结肠炎中的1型辅助性T细胞趋化因子

Th1 chemokines in ulcerative colitis.

作者信息

Ragusa F

机构信息

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

出版信息

Clin Ter. 2015;166(2):e126-31. doi: 10.7417/CT.2015.1835.

Abstract

Many studies have shown that chemokine (C-X-C motif) receptor (CXCR)3 (a chemokine receptor in the CXC family) and its ligand chemokines, monokine induced by interferon (IFN)-γ(MIG), IFN-γ-inducible protein 10 (IP-10) and IFN-inducible T-cell α chemoattractant (I-TAC), are strongly overexpressed in the intestinal mucosa of mice with experimental colitis, and in patients with ulcerative colitis (UC) both in lymphocytes, in macrophages and in epithelial cells. IFN-γ induces CXCR3 and its chemokines expression in epithelial colonic cells; MIG, IP-10 and I-TAC are important for the recruitment of granulocytes and mononuclear cells and thus for the maintenance of inflammation in UC. Serum IP-10 levels reflected UC disease activity, and it may be a marker for the responsiveness of patients to treatments. Recently, a phase II study suggested that an anti-IP-10 antibody, BMS-936557, is a potentially effective therapy for moderately-to-severely active UC.

摘要

许多研究表明,趋化因子(C-X-C基序)受体(CXCR)3(CXC家族中的一种趋化因子受体)及其配体趋化因子,即干扰素(IFN)-γ诱导的单核因子(MIG)、IFN-γ诱导蛋白10(IP-10)和IFN诱导的T细胞α趋化因子(I-TAC),在实验性结肠炎小鼠的肠黏膜中以及溃疡性结肠炎(UC)患者的淋巴细胞、巨噬细胞和上皮细胞中均强烈过表达。IFN-γ可诱导结肠上皮细胞中CXCR3及其趋化因子的表达;MIG、IP-10和I-TAC对于粒细胞和单核细胞的募集很重要,因此对于UC炎症的维持也很重要。血清IP-10水平反映了UC的疾病活动,它可能是患者对治疗反应性的一个标志物。最近,一项II期研究表明,抗IP-10抗体BMS-936557是中重度活动性UC的一种潜在有效疗法。

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