| First Author | Sun Y | Year | 2014 |
| Journal | Nat Commun | Volume | 5 |
| Pages | 5225 | PubMed ID | 25301163 |
| Mgi Jnum | J:241204 | Mgi Id | MGI:5897978 |
| Doi | 10.1038/ncomms6225 | Citation | Sun Y, et al. (2014) The mediator subunit Med23 contributes to controlling T-cell activation and prevents autoimmunity. Nat Commun 5:5225 |
| abstractText | T-cell activation is critical for successful immune responses and is controlled at multiple levels. Although many changes of T-cell receptor-associated signalling molecules affect T-cell activation, the transcriptional mechanisms that control this process remain largely unknown. Here we find that T cell-specific deletion of the mediator subunit Med23 leads to hyperactivation of T cells and aged Med23-deficient mice exhibit an autoimmune syndrome. Med23 specifically and consistently promotes the transcription of multiple negative regulators of T-cell activation. In the absence of Med23, the T-cell activation threshold is lower, which results in enhanced antitumour T-cell function. Cumulatively, our data suggest that Med23 contributes to controlling T-cell activation at the transcriptional level and prevents the development of autoimmunity. |
