Journal
NATURE IMMUNOLOGY
Volume 12, Issue 1, Pages 86-U114Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1965
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- National Institute of Dental and Craniofacial Research (US National Institutes of Health)
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [ZIADE000101, ZIADE000551] Funding Source: NIH RePORTER
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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-beta 1 (TGF-beta 1)-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.
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