Huan Jianya, Culbertson Nicole, Spencer Leslie, Bartholomew Richard, Burrows Gregory G, Chou Yuan K, Bourdette Dennis, Ziegler Steven F, Offner Halina, Vandenbark Arthur A
Department of Neurology, Oregon Health and Science University, Portland, Oregon, USA.
J Neurosci Res. 2005 Jul 1;81(1):45-52. doi: 10.1002/jnr.20522.
Autoimmune diseases such as multiple sclerosis (MS) may result from the failure of tolerance mechanisms to prevent expansion of pathogenic T cells. Our study is the first to establish that MS patients have abnormalities in FOXP3 message and protein expression levels in peripheral CD4+ CD25+ T cells (Tregs) that are quantitatively related to a reduction in functional suppression induced during suboptimal T-cell receptor (TCR) ligation. Of importance, this observation links a defect in functional peripheral immunoregulation to an established genetic marker that has been unequivocally shown to be involved in maintaining immune tolerance and preventing autoimmune diseases. Diminished FOXP3 levels thus indicate impaired immunoregulation by Tregs that may contribute to MS. Future studies will evaluate the effects of therapies known to influence Treg cell function and FOXP3 expression, including TCR peptide vaccination and supplemental estrogen.
自身免疫性疾病,如多发性硬化症(MS),可能是由于耐受机制无法阻止致病性T细胞的扩增所致。我们的研究首次证实,MS患者外周CD4+ CD25+ T细胞(调节性T细胞,Tregs)中的FOXP3信使核糖核酸和蛋白表达水平存在异常,且这些异常与次优T细胞受体(TCR)连接过程中诱导的功能抑制降低在数量上相关。重要的是,这一观察结果将功能性外周免疫调节缺陷与一个已明确显示参与维持免疫耐受和预防自身免疫性疾病的既定遗传标记联系起来。因此,FOXP3水平降低表明调节性T细胞的免疫调节受损,这可能导致MS。未来的研究将评估已知影响调节性T细胞功能和FOXP3表达的疗法的效果,包括TCR肽疫苗接种和补充雌激素。