Pillemer Brendan B L, Xu Hui, Oriss Timothy B, Qi Zengbiao, Ray Anuradha
Department of Medicine, Pulmonary, Allergy and Critical Care Division, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Eur J Immunol. 2007 Aug;37(8):2082-9. doi: 10.1002/eji.200737193.
Naturally occurring CD4+CD25+FoxP3+ regulatory T cells (Treg) suppress T helper (Th) cell-mediated immune responses. The cytokines IL-2 and IL-6 are known to influence Treg function. However, their relative effects on Th cells versus Treg are not well understood. Stimulation with IL-2, and to a lesser extent, IL-6, enhanced Treg proliferation, FoxP3 and CTLA4 maintenance, and suppressive function. In contrast, when IL-2 or IL-6 were added to Treg/Th cell cocultures, suppression was inhibited. The molecule SOCS3 negatively regulates responses to IL-2 and IL-6. Interestingly, unlike Th cells, Treg were found to be deficient in SOCS3 protein expression. The significance of this finding lies in the need for Treg to rapidly respond to these cytokines to prevent unwarranted immune responses to self-antigens. Overexpression of SOCS3 in Treg decreased their proliferation, FoxP3 and CTLA-4 expression and suppressive function. Thus, up-regulation of SOCS3 expression may be a useful therapeutic approach in diseases where inhibition of Treg is desirable.
天然存在的CD4+CD25+FoxP3+调节性T细胞(Treg)可抑制辅助性T(Th)细胞介导的免疫反应。已知细胞因子IL-2和IL-6会影响Treg功能。然而,它们对Th细胞和Treg的相对影响尚未得到充分了解。用IL-2刺激,以及在较小程度上用IL-6刺激,可增强Treg增殖、FoxP3和CTLA4维持以及抑制功能。相反,当将IL-2或IL-6添加到Treg/Th细胞共培养物中时,抑制作用受到抑制。分子SOCS3对IL-2和IL-6的反应起负调节作用。有趣的是,与Th细胞不同,发现Treg缺乏SOCS3蛋白表达。这一发现的意义在于Treg需要对这些细胞因子快速做出反应,以防止对自身抗原产生不必要的免疫反应。Treg中SOCS3的过表达降低了它们的增殖、FoxP3和CTLA-4表达以及抑制功能。因此,上调SOCS3表达可能是在需要抑制Treg的疾病中一种有用的治疗方法。