Other
13 Authors
- Zamarron BF,
- Konkel JE,
- Vaque JP,
- Yu D,
- Maruyama T,
- Wang W,
- Li J,
- Zhang P,
- Zhang B,
- Wu Y,
- Zhuang Y,
- Chen W,
- Gutkind JS
First Author | Maruyama T | Year | 2011 |
Journal | Nat Immunol | Volume | 12 |
Issue | 1 | Pages | 86-95 |
PubMed ID | 21131965 | Mgi Jnum | J:167447 |
Mgi Id | MGI:4868301 | Doi | 10.1038/ni.1965 |
Citation | Maruyama T, et al. (2011) Control of the differentiation of regulatory T cells and T(H)17 cells by the DNA-binding inhibitor Id3. Nat Immunol 12(1):86-95 |
abstractText | The molecular mechanisms that direct transcription of the gene encoding the transcription factor Foxp3 in CD4(+) T cells remain ill-defined. We show here that deletion of the DNA-binding inhibitor Id3 resulted in the defective generation of Foxp3(+) regulatory T cells (T(reg) cells). We identify two transforming growth factor-beta1 (TGF-beta1)-dependent mechanisms that were vital for activation of Foxp3 transcription and were defective in Id3(-/-) CD4(+) T cells. Enhanced binding of the transcription factor E2A to the Foxp3 promoter promoted Foxp3 transcription. Id3 was required for relief of inhibition by the transcription factor GATA-3 at the Foxp3 promoter. Furthermore, Id3(-/-) T cells showed greater differentiation into the T(H)17 subset of helper T cells in vitro and in a mouse asthma model. Therefore, a network of factors acts in a TGF-beta-dependent manner to control Foxp3 expression and inhibit the development of T(H)17 cells. |