Cutting edge:: IL-2 is essential for TGF-β-mediated induction of Foxp3+ T regulatory cells

被引:397
作者
Davidson, Todd S. [1 ]
DiPaolo, Richard J. [1 ]
Andersson, John [1 ]
Shevach, Ethan M. [1 ]
机构
[1] NIAID, Cellular Immunol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA
关键词
D O I
10.4049/jimmunol.178.7.4022
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
TGF-beta is a pluripotent cytokine that is capable of inducing the expression of Foxp3 in naive T lymphocytes. TGF-beta-induced cells are phenotypically similar to thymic-derived regulatory T cells in that they are anergic and suppressive. We have examined the cytokine and costimulatory molecule requirements for TGF-beta-mediated induction and maintenance of Foxp3 by CD4(+)Foxp3(-) cells. IL-2 plays a non-redundant role in TGF-beta-induced Foxp3 expression. Other common gamma-chain-utilizing, cytokines were unable to induce Foxp3 expression in IL-2-deficient T cells. The role of CD28 in the induction of Foxp3 was solely related to its capacity to enhance the endogenous production of IL-2. Toxp3 expression was stable in vitro and in vivo in the absence of IL-2. As TGF-beta-induced T regulatory cells can be easily grown in vitro, they may prove useful for the treatment of autoimmune diseases, for the prevention of graft rejection, and graft versus host disease.
引用
收藏
页码:4022 / 4026
页数:5
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