| First Author | Wu C | Year | 2017 |
| Journal | Nat Immunol | Volume | 18 |
| Issue | 3 | Pages | 344-353 |
| PubMed ID | 28114290 | Mgi Jnum | J:259014 |
| Mgi Id | MGI:6140942 | Doi | 10.1038/ni.3667 |
| Citation | Wu C, et al. (2017) The transcription factor musculin promotes the unidirectional development of peripheral Treg cells by suppressing the TH2 transcriptional program. Nat Immunol 18(3):344-353 |
| abstractText | Although master transcription factors (TFs) are key to the development of specific T cell subsets, whether additional transcriptional regulators are induced by the same stimuli that dominantly repress the development of other, non-specific T cell lineages has not been fully elucidated. Through the use of regulatory T cells (Treg cells) induced by transforming growth factor-beta (TGF-beta), we identified the TF musculin (MSC) as being critical for the development of induced Treg cells (iTreg cells) by repression of the T helper type 2 (TH2) transcriptional program. Loss of MSC reduced expression of the Treg cell master TF Foxp3 and induced TH2 differentiation even under iTreg-cell-differentiation conditions. MSC interrupted binding of the TF GATA-3 to the locus encoding TH2-cell-related cytokines and diminished intrachromosomal interactions within that locus. MSC-deficient (Msc(-/-)) iTreg cells were unable to suppress TH2 responses, and Msc(-/-) mice spontaneously developed gut and lung inflammation with age. MSC therefore enforced Foxp3 expression and promoted the unidirectional induction of iTreg cells by repressing the TH2 developmental program. |
