Abstract
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 ±-chain (IL-7R±) 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.
Original language | English (US) |
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Pages (from-to) | 544-550 |
Number of pages | 7 |
Journal | Nature Immunology |
Volume | 12 |
Issue number | 6 |
DOIs | |
State | Published - Jun 2011 |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology