| First Author | Luo X | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 5 | Pages | 2757-61 |
| PubMed ID | 18292494 | Mgi Jnum | J:131730 |
| Mgi Id | MGI:3774252 | Doi | 10.4049/jimmunol.180.5.2757 |
| Citation | Luo X, et al. (2008) Cutting Edge: TGF-{beta}-Induced Expression of Foxp3 in T cells Is Mediated through Inactivation of ERK. J Immunol 180(5):2757-61 |
| abstractText | The peripheral induction of T regulatory cells can be accomplished by TGF-beta through an epigenetic regulation leading to the expression of Foxp3. However, the exact mechanism of such a TGF-beta-mediated action remains unclear. In the current study, we found that TGF-beta 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-beta 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-beta-induced expression of Foxp3 may be mediated through the inactivation of ERK. |
