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简要探讨趋化因子单核细胞蛋白-1(CCL2)在银屑病病理生理学中的作用。

A brief look at the role of monocyte chemoattractant protein-1 (CCL2) in the pathophysiology of psoriasis.

机构信息

Department of Dermatology, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

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

出版信息

Cytokine. 2018 Oct;110:226-231. doi: 10.1016/j.cyto.2017.12.010. Epub 2017 Dec 23.

DOI:10.1016/j.cyto.2017.12.010
PMID:29277337
Abstract

Psoriasis (PsO) is a chronic skin disorder resulting from the imbalanced interactionbetween infiltrating immune cells and keratinocytes. These immune cells, including monocytes, are able to mediate the immune responses in inflamed skin lesions. Chemokines are responsible for the recruitment of leukocytes to sites of inflammation. In patients with PsO, the keratinocytes are the main source of monocyte chemotactic protein 1 (MCP-1/CCL2), which is a CC chemokine. After CCL2 binds to the chemokine receptor CCR2, which mainly is expressed on the surface of monocytes, the monocytes differentiate into macrophages and migrate from the blood stream to sites of inflammation. This process can cause the formation of lesions. Accordingly, it has been hypothesized that CCL2 could be a potential biomarker to monitor the progression of PsO. Thus, evidence suggests that there could be a potential role for CCR2 and CCL2 during treatment of PsO and to prevent its further development. For example, to modify the course of PsO, efforts have been made to inhibit or modulate the CCR2/CCL2 axis. However, before exploring the targeting of the CCR2/CCL2 axis in a clinical setting, better understanding of the different molecular aspects of PsO is required.

摘要

银屑病(PsO)是一种慢性皮肤疾病,源于浸润免疫细胞与角质形成细胞之间失衡的相互作用。这些免疫细胞,包括单核细胞,能够在炎症皮肤损伤中介导免疫反应。趋化因子负责将白细胞募集到炎症部位。在银屑病患者中,角质形成细胞是单核细胞趋化蛋白 1(MCP-1/CCL2)的主要来源,MCP-1/CCL2 是一种 CC 趋化因子。CCL2 与主要表达在单核细胞表面的趋化因子受体 CCR2 结合后,单核细胞分化为巨噬细胞并从血液迁移到炎症部位。这个过程会导致损伤的形成。因此,人们假设 CCL2 可能是监测银屑病进展的潜在生物标志物。因此,有证据表明,在治疗银屑病和防止其进一步发展时,CCR2 和 CCL2 可能发挥潜在作用。例如,为了改变银屑病的病程,人们努力抑制或调节 CCR2/CCL2 轴。然而,在探索 CCR2/CCL2 轴在临床环境中的靶向作用之前,需要更好地了解银屑病的不同分子方面。

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