Journal
NATURE IMMUNOLOGY
Volume 14, Issue 11, Pages 1155-U79Publisher
NATURE PORTFOLIO
DOI: 10.1038/ni.2710
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Funding
- National Health and Medical Research Council of Australia
- Sylvia and Charles Viertel Foundation
- Howard Hughes Medical Institute
- Australian Research Council
- National Heart Foundation
- The Walter and Eliza Hall Institute Genomics Fund
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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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