溃疡性结肠炎中的 CCL5/CCR5 轴

IF 3.7 4区 医学 Q2 CELL BIOLOGY
Fan Fan Qu , Ya Qian Wu , Jian Bin Ji , Lin Yan , Jing Jing Wei , Qing Chao Song , Bao Qing Xu , Ming Cheng , Zheng Hua Zhou
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引用次数: 0

摘要

溃疡性结肠炎(UC)是一种慢性非特异性炎症性肠病,主要特征是肠粘膜的炎性变化。虽然溃疡性结肠炎的具体病因尚不清楚,但一般认为它与多种因素有关,其中参与促炎和抗炎过程的分子表达失衡可导致溃疡性结肠炎。CCL5(C-C 趋化因子配体 5)是关键的促炎因子之一,在包括 UC 在内的各种炎症性疾病中发挥着不可或缺的作用。CCL5 可结合并激活受体 CCR5(C-C 趋化因子受体 5 型),进而促进 PI3K/AKT、NF-κB 和 Ras/MAPK 等信号通路,在 UC 的发病机制中发挥重要作用。本文的重点是 CCL5/CCR5 轴及其后续信号通路在 UC 治疗中的功能。除此之外,文章还进一步探讨了针对 CCL5/CCR5 轴的 CCR5 拮抗剂和激动剂在治疗 UC 方面可能带来的疗效。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The CCL5/CCR5 axis in ulcerative colitis

The CCL5/CCR5 axis in ulcerative colitis
Ulcerative colitis (UC) is a chronic nonspecific inflammatory bowel disease characterized mainly by inflammatory changes in the intestinal mucosa. While the specific etiology of UC remains unclear, it is generally believed that it is related to many factors, among which the imbalance in the expression of molecules involved in pro-inflammatory and anti-inflammatory processes can lead to UC. CCL5 (C–C chemokine ligand 5) is one of the key pro-inflammatory factors and plays an indispensable role in various inflammatory diseases, including UC. CCL5 binds and activates the receptor CCR5 (C–C chemokine receptor type 5), which in turn, promotes signaling pathways such as PI3K/AKT, NF-κB, and Ras/MAPK, playing an important role in the pathogenesis of UC. The focus of this paper is on the function of the CCL5/CCR5 axis and its subsequent signaling pathways in UC therapy. In addition to this, the article further explores the possible healing benefits of CCR5 antagonists and agonists aimed at the CCL5/CCR5 axis for UC treatment.
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来源期刊
Cellular immunology
Cellular immunology 生物-免疫学
CiteScore
8.20
自引率
2.30%
发文量
102
审稿时长
30 days
期刊介绍: Cellular Immunology publishes original investigations concerned with the immunological activities of cells in experimental or clinical situations. The scope of the journal encompasses the broad area of in vitro and in vivo studies of cellular immune responses. Purely clinical descriptive studies are not considered. Research Areas include: • Antigen receptor sites • Autoimmunity • Delayed-type hypersensitivity or cellular immunity • Immunologic deficiency states and their reconstitution • Immunologic surveillance and tumor immunity • Immunomodulation • Immunotherapy • Lymphokines and cytokines • Nonantibody immunity • Parasite immunology • Resistance to intracellular microbial and viral infection • Thymus and lymphocyte immunobiology • Transplantation immunology • Tumor immunity.
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