Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, 410011 Hunan, China.
Division of Allergy, Asthma and Immunology, Department of Pediatrics, Thomas Jefferson University Hospital, USA.
Clin Immunol. 2014 Jan;150(1):22-30. doi: 10.1016/j.clim.2013.10.009. Epub 2013 Oct 25.
Psoriasis vulgaris (PV) is a chronic inflammatory and T cell-mediated autoimmune skin disease. An immune dysfunction that is manifested by abnormally activated T cells and defective regulatory T (Treg) cells may play an important role in the pathogenesis of PV. However, the precise mechanism of the immune dysfunction in PV patients still remains unclear. In this study, we found that miR-210 expression is increased significantly in CD4(+) T cells from patients with PV and confirmed that FOXP3 is a target gene of miR-210. We also found that overexpression of miR-210 inhibits FOXP3 expression and impairs the immunosuppressive functions of Treg cells in CD4(+) T cells from healthy controls. In contrast, inhibition of miR-210 increases FOXP3 expression and reverses the immune dysfunction in CD4(+) T cells from patients with PV. Our data demonstrates that increased miR-210 induces immune dysfunction via by FOXP3 in CD4(+) T cells from patients with PV.
寻常型银屑病（PV）是一种慢性炎症性和 T 细胞介导的自身免疫性皮肤病。免疫功能紊乱，表现为异常激活的 T 细胞和功能缺陷的调节性 T（Treg）细胞，可能在 PV 的发病机制中发挥重要作用。然而，PV 患者免疫功能紊乱的确切机制仍不清楚。在本研究中，我们发现 miR-210 在 PV 患者的 CD4+T 细胞中表达显著增加，并证实 FOXP3 是 miR-210 的靶基因。我们还发现，miR-210 的过表达抑制 FOXP3 的表达，并损害来自健康对照者的 CD4+T 细胞中的 Treg 细胞的免疫抑制功能。相反，抑制 miR-210 增加了 FOXP3 的表达，并逆转了来自 PV 患者的 CD4+T 细胞中的免疫功能紊乱。我们的数据表明，miR-210 的增加通过 FOXP3 在来自 PV 患者的 CD4+T 细胞中诱导免疫功能紊乱。
