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实验性自身免疫性脑脊髓炎(EAE)是由CD4+T细胞介导的自身免疫性中枢神经系统脱髓鞘炎症。以往认为,中和CXC趋化因子受体3(CXCR3)或其配体(CXCL10)可以缓解EAE的病情,减少复发。但近年来研究发现CXCR3或CX-CL10基因敲除能够加重EAE病情,提示它们可能对EAE起保护性作用。本文就CXCR3及其配体CXCL10与EAE的发生发展之间的联系以及相关的调节机制进行综述,为CXCR3受体拮抗剂或CXCL10中和剂在临床上的应用提供理论参考。
Experimental Autoimmune Encephalomyelitis (EAE) is an autoimmune central nervous system demyelinating inflammation mediated by CD4 + T cells. Historically, neutralization of CXCR3 or its ligand (CXCL10) could relieve EAE and reduce recurrence. However, recent studies have found CXCR3 or CX-CL10 knockout can aggravate EAE, suggesting that they may play a protective role in EAE. This review summarizes the linkages between CXCR3 and its ligand CXCL10 and the development of EAE, as well as the relevant regulatory mechanisms, providing a theoretical reference for the clinical application of CXCR3 receptor antagonists or CXCL10 neutralizers.