期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 108, 期 36, 页码 14885-14889出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1105133108
关键词
AP-1; chromatin remodeling; glycolysis; oxidative phosphorylation
资金
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan
- Grants-in-Aid for Scientific Research [21300118] Funding Source: KAKEN
CD8 T cells play a critical role in protection against viral infections. During effector differentiation, CD8 T cells dramatically change chromatin structure and cellular metabolism, but how energy production increases in response to these epigenetic changes is unknown. We found that loss of basic leucine zipper transcription factor, ATF-like (BATF) inhibited effector CD8 T-cell differentiation. At the late effector stage, BATF was induced by IL-12 and required for IL-12-mediated histone acetylation and survival of effector T cells. BATF, together with c-Jun, transcriptionally inhibited expression of the nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase Sirt1, resulting in increased histone acetylation of the T-bet locus and increased cellular NAD(+), which increased ATP production. In turn, high levels of T-bet expression and ATP production promoted effector differentiation and cell survival. These results suggest that BATF promotes effector CD8 T-cell differentiation by regulating both epigenetic remodeling and energy metabolism through Sirt1 expression.
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