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CCL2/CCR2 轴在类风湿关节炎免疫发病机制中的作用:最新证据和治疗方法。

Role of CCL2/CCR2 axis in the immunopathogenesis of rheumatoid arthritis: Latest evidence and therapeutic approaches.

机构信息

Student Research Committee, Rafsanjan University of Medical Sciences, Rafsanjan, Iran; Department of Immunology, School of Medicine; Molecular Medicine Research Center, Institute of Basic Medical Sciences Research, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

Department of Immunology, School of Medicine; Molecular Medicine Research Center, Institute of Basic Medical Sciences Research, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

出版信息

Life Sci. 2021 Mar 15;269:119034. doi: 10.1016/j.lfs.2021.119034. Epub 2021 Jan 13.

DOI:10.1016/j.lfs.2021.119034
PMID:33453247
Abstract

Evidence suggests that uncontrolled immune system responses and their components play a significant role in developing rheumatoid arthritis (RA), which is considered an autoimmune disease (AD). Among immune system mediators, cytokines and chemokines are involved in numerous physiological and pathological processes. CCL2 or monocyte chemoattractant protein-1 (MCP-1) is known as a CC chemokine that can induce the locomotion and recruitment of monocytes and macrophages to the site of injury. When CCL2 binds to its receptors, the most important of which is CCR2, various signaling pathways are triggered, eventually leading to various immunological events such as inflammation. This chemokine also participates in several events involved in RA pathogenesis, such as osteoclastogenesis, migration of effector T cells to the RA synovium tissue, and angiogenesis. In this review article, the role of the CCL2/CCR2 axis in RA pathogenesis and the immunotherapy opportunities based on CCL2/CCR2 axis targeting has been discussed based on existing investigations.

摘要

有证据表明,免疫系统的失控反应及其成分在类风湿关节炎(RA)的发生中起着重要作用,RA 被认为是一种自身免疫性疾病(AD)。在免疫系统介质中,细胞因子和趋化因子参与了许多生理和病理过程。CCL2 或单核细胞趋化蛋白-1(MCP-1)被称为 CC 趋化因子,可诱导单核细胞和巨噬细胞向损伤部位迁移和募集。当 CCL2 与其受体结合时,其中最重要的是 CCR2,会触发各种信号通路,最终导致各种免疫事件,如炎症。这种趋化因子还参与 RA 发病机制中的几个事件,如破骨细胞生成、效应 T 细胞向 RA 滑膜组织的迁移和血管生成。在这篇综述文章中,根据现有的研究,讨论了 CCL2/CCR2 轴在 RA 发病机制中的作用以及基于 CCL2/CCR2 轴靶向的免疫治疗机会。

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