期刊
JOURNAL OF IMMUNOLOGY
卷 190, 期 9, 页码 4585-4594出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1300099
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资金
- National Health and Medical Research Council of Australia
- Wellcome Trust
- Viertel Foundation
- Howard Hughes Medical Institute
- Australian Research Council
- Boehringer Ingelheim
- Genome Research in Austria initiative
- Bundesminsterium fur Bildung und Wissenschaft
- Victorian State Government
- Australian Government National Health and Medical Research Council Independent Research Institute Infrastructure Support Scheme
The transcription factor inhibitor of DNA binding (Id) 2 modulates T cell fate decisions, but the molecular mechanism underpinning this regulation is unclear. In this study we show that loss of Id2 cripples effector differentiation and instead programs CD8(+) T cells to adopt a memory fate with increased Eomesodermin and Tcf7 expression. We demonstrate that Id2 restrains CD8(+) T cell memory differentiation by inhibiting E2A-mediated direct activation of Tcf7 and that Id2 expression level mirrors T cell memory recall capacity. As a result of the defective effector differentiation, Id2-deficient CD8(+) T cells fail to induce sufficient Tbx21 expression to generate short-lived effector CD8(+) T cells. Our findings reveal that the Id2/E2A axis orchestrates T cell differentiation through the induction or repression of downstream transcription factors essential for effector and memory T cell differentiation. The Journal of Immunology, 2013, 190: 4585-4594.
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