| First Author | Man K | Year | 2013 |
| Journal | Nat Immunol | Volume | 14 |
| Issue | 11 | Pages | 1155-65 |
| PubMed ID | 24056747 | Mgi Jnum | J:208205 |
| Mgi Id | MGI:5562481 | Doi | 10.1038/ni.2710 |
| Citation | Man K, et al. (2013) The transcription factor IRF4 is essential for TCR affinity-mediated metabolic programming and clonal expansion of T cells. Nat Immunol 14(11):1155-65 |
| abstractText | During immune responses, T cells are subject to clonal competition, which leads to the predominant expansion of high-affinity clones; however, there is little understanding of how this process is controlled. We found here that the transcription factor IRF4 was induced in a manner dependent on affinity for the T cell antigen receptor (TCR) and acted as a dose-dependent regulator of the metabolic function of activated T cells. IRF4 regulated the expression of key molecules required for the aerobic glycolysis of effector T cells and was essential for the clonal expansion and maintenance of effector function of antigen-specific CD8(+) T cells. Thus, IRF4 is an indispensable molecular 'rheostat' that 'translates' TCR affinity into the appropriate transcriptional programs that link metabolic function with the clonal selection and effector differentiation of T cells. |
