Tran Dat Q, Ramsey Heather, Shevach Ethan M
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Blood. 2007 Oct 15;110(8):2983-90. doi: 10.1182/blood-2007-06-094656. Epub 2007 Jul 20.
Thymic-derived natural T-regulatory cells (nTregs) are important for the induction of self-tolerance and the control of autoimmunity. Murine CD4+CD25(-)Foxp3(-) cells can be induced to express Foxp3 after T-cell receptor (TCR) activation in the presence of transforming growth factor beta (TGFbeta) and are phenotypically similar to nTregs. Some studies have suggested that TCR stimulation of human CD4+CD25(-) cells results in the induction of transient expression of FOXP3, but that the induced cells lack a regulatory phenotype. We demonstrate here that TCR stimulation alone was insufficient to induce FOXP3 expression in the absence of TGFbeta, whereas high levels of FOXP3 expression could be induced in the presence of TGFbeta. Although FOXP3 expression was stable, the TGFbeta-induced FOXP3+ T cells were neither anergic nor suppressive and produced high levels of effector cytokines. These results suggest that even high levels of FOXP3 expression are insufficient to define a human CD4+ T cell as a T-regulatory cell.
胸腺来源的天然T调节细胞(nTregs)对于诱导自身耐受和控制自身免疫至关重要。在转化生长因子β(TGFβ)存在的情况下,小鼠CD4 + CD25(-)Foxp3(-)细胞在T细胞受体(TCR)激活后可被诱导表达Foxp3,并且在表型上与nTregs相似。一些研究表明,TCR刺激人CD4 + CD25(-)细胞会导致FOXP3短暂表达的诱导,但诱导的细胞缺乏调节表型。我们在此证明,在没有TGFβ的情况下,单独的TCR刺激不足以诱导FOXP3表达,而在TGFβ存在的情况下可以诱导高水平的FOXP3表达。尽管FOXP3表达稳定,但TGFβ诱导的FOXP3 + T细胞既无反应性也无抑制性,并且产生高水平的效应细胞因子。这些结果表明,即使高水平的FOXP3表达也不足以将人CD4 + T细胞定义为T调节细胞。