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CCRL2在实验性自身免疫性脑脊髓炎(EAE)恢复阶段调节M1/M2极化。

CCRL2 regulates M1/M2 polarization during EAE recovery phase.

作者信息

Mazzon Cristina, Zanotti Lucia, Wang Li, Del Prete Annalisa, Fontana Elena, Salvi Valentina, Poliani Pietro Luigi, Sozzani Silvano

机构信息

Department of Molecular and Translational Medicine, University of Brescia, Italy; and Humanitas Clinical and Research Center, Rozzano, Italy.

Humanitas Clinical and Research Center, Rozzano, Italy.

出版信息

J Leukoc Biol. 2016 Jun;99(6):1027-33. doi: 10.1189/jlb.3MA0915-444RR. Epub 2016 Jan 7.

DOI:10.1189/jlb.3MA0915-444RR
PMID:26744451
Abstract

Chemokine (CC motif) receptor-like 2 is a 7-transmembrane protein related to the family of the atypical chemokine receptors, which are proteins devoid of chemotactic activity and involved in the control of inflammation. Experimental autoimmune encephalitis is an autoimmune disorder that replicates the inflammatory aspects of multiple sclerosis. Chemokine (CC motif) receptor-like 2-deficient mice developed exacerbated, nonresolving disease with protracted inflammatory response and increased demyelination. The increased severity of the disease was associated with higher levels of microglia/macrophage activation markers and imbalanced M1/M2 polarization. Thus, chemokine (CC motif) receptor-like 2 is involved in the downregulation of central nervous system-associated experimental autoimmune encephalitis inflammation in the recovery phase of the disease. Therefore chemokine (CC motif) receptor-like 2 should be considered to be a molecule involved in the regulation of the inflammatory response associated with multiple sclerosis.

摘要

趋化因子(CC基序)受体样2是一种与非典型趋化因子受体家族相关的7次跨膜蛋白,这些受体蛋白缺乏趋化活性,但参与炎症控制。实验性自身免疫性脑脊髓炎是一种自身免疫性疾病,可复制多发性硬化症的炎症特征。缺乏趋化因子(CC基序)受体样2的小鼠会出现病情加重、无法缓解的疾病,伴有持续的炎症反应和脱髓鞘增加。疾病严重程度的增加与小胶质细胞/巨噬细胞激活标志物水平升高以及M1/M2极化失衡有关。因此,趋化因子(CC基序)受体样2在疾病恢复阶段参与中枢神经系统相关实验性自身免疫性脑脊髓炎炎症的下调。因此,应将趋化因子(CC基序)受体样2视为参与调节与多发性硬化症相关炎症反应的分子。

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