Journal
NATURE IMMUNOLOGY
Volume 12, Issue 6, Pages 544-U246Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2034
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Funding
- National Institutes of Health [1K22AI070317-01A1]
- American Cancer Society [114937-IRG-96-153-07-IRG]
- Wistar Cancer Center [P30 CA10815]
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The molecular mechanisms that underlie T cell quiescence are poorly understood. Here we report that mature naive CD8(+) T cells lacking the transcription factor Foxp1 gained effector phenotype and function and proliferated directly in response to interleukin 7 (IL-7) in vitro. Foxp1 repressed expression of the IL-7 receptor alpha-chain (IL-7R alpha) by antagonizing Foxo1 and negatively regulated signaling by the kinases MEK and Erk. Acute deletion of Foxp1 induced naive T cells to gain an effector phenotype and proliferate in lympho-replete mice. Foxp1-deficient naive CD8(+) T cells proliferated even in lymphopenic mice deficient in major histocompatibility complex class I. Our results demonstrate that Foxp1 exerts essential cell-intrinsic regulation of naive T cell quiescence, providing direct evidence that lymphocyte quiescence is achieved through actively maintained mechanisms that include transcriptional regulation.
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