Wuhan No.1 Hospital, No. 375 Zhongshan Avenue, Wuhan, 430000, China.
J Clin Immunol. 2011 Dec;31(6):1112-9. doi: 10.1007/s10875-011-9559-x. Epub 2011 Jul 6.
Thirty-five rheumatoid arthritis (RA) patients and 27 healthy volunteers were enrolled in the study. Regulatory T (Treg) cell numbers were significantly reduced in RA patients. RA Treg cells exhibited an impaired capacity to inhibit proliferation and cytokine secretion of autologous T effector (Teff) cells. However, the crossover experiments further indicated that this impaired suppression was due to resistance of Teff cells but not to an intrinsic defect of Treg cells in RA patients. RA Teff cells showed a higher expression of membrane tumor necrosis factor-related apoptosis-inducing ligand and secreted more soluble tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). TRAIL could induce apoptosis in Treg cells. Neutralization of TRAIL restored the regulation of Teff by Treg in RA patients. In summary, our data suggest that reduced peripheral Treg cell numbers and an increased resistance of Teff cells to suppression by Treg cells were present in RA patients, and TRAIL may be an underlying mechanism for the impaired regulation of Teff cells by Treg cells.
研究纳入 35 例类风湿关节炎（RA）患者和 27 名健康志愿者。RA 患者调节性 T（Treg）细胞数量显著减少。RA Treg 细胞抑制自身 T 效应（Teff）细胞增殖和细胞因子分泌的能力受损。然而，交叉实验进一步表明，这种抑制受损是由于 Teff 细胞的抵抗，而不是 RA 患者 Treg 细胞的内在缺陷。RA Teff 细胞表面肿瘤坏死因子相关凋亡诱导配体（TRAIL）表达较高，分泌更多可溶性 TRAIL。TRAIL 可诱导 Treg 细胞凋亡。TRAIL 的中和恢复了 RA 患者 Treg 对 Teff 的调节。总之，我们的数据表明，RA 患者外周 Treg 细胞数量减少，Teff 细胞对 Treg 细胞抑制的抵抗力增加，TRAIL 可能是 Treg 细胞对 Teff 细胞调节受损的潜在机制。
