Ruffilli I
Department of Clinical and Experimental Medicine, University of Pisa, Italy.
Clin Ter. 2019 Jan-Feb;170(1):e71-e76. doi: 10.7417/CT.2019.2111.
Many studies reported that monokine induced by interferon (IFN)-γ(MIG), and its receptor chemokine (C-X-C motif) receptor (CXCR)3, are expressed by T cells in different types of cutaneous damages associated with lupus, and that the CXCR3-activating chemokines are produced locally, suggesting that they play a significant role in the recruitment of T cells in these inflammatory lesions. Circulating MIG levels are increased in cutaneous Systemic Lupus Erythematosus (SLE) patients and strongly correlated with the disease activity. The data discussed in this review show that there is an increasing evidence that MIG may participate in the pathogenesis of a variety of the manifestations of cutaneous SLE, even if the exact role of MIG in the pathogenesis of this disease remains to be clarified.
许多研究报告称，干扰素（IFN）-γ诱导的单核细胞趋化蛋白（MIG）及其受体趋化因子（C-X-C基序）受体（CXCR）3在与狼疮相关的不同类型皮肤损伤的T细胞中表达，且CXCR3激活趋化因子在局部产生，这表明它们在这些炎症性病变中T细胞的募集中起重要作用。皮肤型系统性红斑狼疮（SLE）患者的循环MIG水平升高，且与疾病活动度密切相关。本综述中讨论的数据表明，越来越多的证据显示MIG可能参与皮肤型SLE多种表现的发病机制，尽管MIG在该疾病发病机制中的确切作用仍有待阐明。
