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Nat Immunol. 2013 Nov;14(11):1155-65. doi: 10.1038/ni.2710. Epub 2013 Sep 22.

The transcription factor IRF4 is essential for TCR affinity-mediated metabolic programming and clonal expansion of T cells.

Author information

1] The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia. [2] The Department of Medical Biology, University of Melbourne, Parkville, Australia.

Erratum in

  • Nat Immunol. 2014 Sep;15(9):894.


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.

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