Cutting edge: TGF-β-induced expression of Foxp3 in T cells is mediated through inactivation of ERK

Xunrong Luo*, Qiang Zhang, Victoria Liu, Zhenbiao Xia, Kathryn L. Pothoven, Chung Lee

*Corresponding author for this work

Research output: Contribution to journalArticle

56 Scopus citations

Abstract

The peripheral induction of T regulatory cells can be accomplished by TGF-β through an epigenetic regulation leading to the expression of Foxp3. However, the exact mechanism of such a TGF-β-mediated action remains unclear. In the current study, we found that TGF-β treatment of CD4 +CD25- T cells during T cell activation led to a transient inhibition of the phosphorylation of ERK followed by the induction of Foxp3 expression in these cells. Direct treatment with a specific ERK inhibitor, UO126, during CD4+CD25- T cell activation also induced Foxp3 expression and conferred a suppressive function to the induced Foxp3 + T cells. Furthermore, treatment of T cells with either TGF-β or UO126 significantly down-regulated the expression of DNMTs, a reaction normally elicited by demethylation agents, such as 5-Aza-2′-deoxycytidine. These results indicate that the epigenetic regulation of TGF-β-induced expression of Foxp3 may be mediated through the inactivation of ERK.

Original languageEnglish (US)
Pages (from-to)2757-2761
Number of pages5
JournalJournal of Immunology
Volume180
Issue number5
StatePublished - Mar 1 2008

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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