The First Affiliated Hospital of Chongqing Medical University, People's Republic of China.
Invest Ophthalmol Vis Sci. 2012 Feb 27;53(2):1012-7. doi: 10.1167/iovs.11-8505.
IL-7/IL-7R has been found to be involved in the pathogenesis of several autoimmune diseases. This study was designed to investigate the potential role of IL-7/IL-7R in the pathogenesis of Vogt Koyanagi-Harada (VKH), an organ-specific autoimmune disease.
IL-7 was measured with an enzyme-linked immunosorbent assay (ELISA) in serum obtained from patients with active or inactive VKH and from healthy individuals. The expression of IL-7R was measured by flow cytometry (FCM). Cell proliferation was determined after exposure of peripheral blood mononuclear cells (PBMCs) and CD4(+) T cells to recombinant IL-7. The levels of IL-17 and IFN-γ levels were detected by ELISA after these cells were cocultured with recombinant IL-7. The influence of recombinant IL-7 on the expansion of Th1 and Th17 cells was evaluated by using FCM.
IL-7 was significantly increased in the serum of patients with active VKH compared with those with inactive VKH (P < 0.001) and normal controls (P < 0.001). However, there was no difference between VKH patients and normal controls in the expression of IL-7Rα on CD4(+) T cells. Recombinant IL-7 induced significant cell proliferation and secretion of IL-17 and IFN-γ by PBMCs and CD4(+) T cells. It furthermore promoted the expansion of both Th1 and Th17 cells.
The findings suggest that IL-7 is involved in the pathogenesis of VKH disease.
IL-7/IL-7R 已被发现参与了几种自身免疫性疾病的发病机制。本研究旨在探讨 IL-7/IL-7R 在 Vogt-小柳-原田(VKH)病发病机制中的潜在作用,VKH 是一种器官特异性自身免疫性疾病。
采用酶联免疫吸附试验(ELISA)检测活动期和静止期 VKH 患者及健康对照者血清中 IL-7 的浓度。采用流式细胞术(FCM)检测 IL-7R 的表达。用重组 IL-7 刺激外周血单个核细胞(PBMCs)和 CD4+T 细胞后,检测细胞增殖。将这些细胞与重组 IL-7 共培养后,通过 ELISA 检测 IL-17 和 IFN-γ 的水平。通过 FCM 评估重组 IL-7 对 Th1 和 Th17 细胞扩增的影响。
与静止期 VKH 患者(P<0.001)和正常对照组(P<0.001)相比,活动期 VKH 患者血清中 IL-7 水平显著升高。然而,CD4+T 细胞上的 IL-7Rα 在 VKH 患者与正常对照组之间无差异。重组 IL-7 可诱导 PBMCs 和 CD4+T 细胞显著增殖,并分泌 IL-17 和 IFN-γ,同时促进 Th1 和 Th17 细胞的扩增。
这些发现提示 IL-7 参与了 VKH 疾病的发病机制。