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• W2078453467 abstract "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. T-cell activation is controlled by signalling through the T-cell receptor and other molecules. Here the authors show that Med23 is a negative regulator of T-cell activation at a transcriptional level and that Med23 deficiency in T cells results in development of autoimmunity in aged mice." @default.
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• W2078453467 date "2014-10-10" @default.
• W2078453467 modified "2023-09-23" @default.
• W2078453467 title "The mediator subunit Med23 contributes to controlling T-cell activation and prevents autoimmunity" @default.
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• W2078453467 doi "https://doi.org/10.1038/ncomms6225" @default.
• W2078453467 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25301163" @default.
• W2078453467 hasPublicationYear "2014" @default.
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