Department of Neurosciences, Institute of Neurology, Catholic University, Rome, Italy.
Hum Immunol. 2010 May;71(5):437-41. doi: 10.1016/j.humimm.2010.01.024. Epub 2010 Feb 14.
A defect of CD4(+) regulatory T cells (Treg) seems to be involved in the pathogenesis of multiple sclerosis (MS). Besides Treg, CD8(+) T cells also can suppress the immune response. Forkhead box p3 (Foxp3) is known to program the acquisition of suppressive capacities in CD4(+) T cells and recent studies showed that in vitro antigen activation leads to Foxp3 expression in CD8(+) T cells, gaining of suppressive activity. By flow cytometry we found a lower percentage of circulating CD8(+)Foxp3(+) T cells in relapsing than in remitting patients with MS and in controls. No significant differences were observed in CD8(+)Foxp3(+) T cell percentage between healthy subjects and patients in remission. Our data suggest that peripheral CD8(+)Foxp3(+) T cells may play a role in the maintenance of tolerance in MS.
CD4(+) 调节性 T 细胞（Treg）的缺陷似乎与多发性硬化症（MS）的发病机制有关。除了 Treg，CD8(+) T 细胞也可以抑制免疫反应。叉头框蛋白 P3（Foxp3）被认为是在 CD4(+) T 细胞中获得抑制能力的编程，最近的研究表明，体外抗原激活导致 CD8(+) T 细胞中 Foxp3 的表达，获得抑制活性。通过流式细胞术，我们发现复发期 MS 患者和对照组患者循环中的 CD8(+)Foxp3(+) T 细胞比例较低，而缓解期患者和对照组患者之间的 CD8(+)Foxp3(+) T 细胞比例没有显著差异。我们的数据表明，外周血 CD8(+)Foxp3(+) T 细胞可能在 MS 中的耐受维持中发挥作用。
