Journal
IMMUNITY
Volume 39, Issue 2, Pages 335-346Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2013.07.016
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Funding
- National Institute of Arthritis, Musculoskeletal, and Skin Diseases [RO1 AR060723]
- Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, USA
- [T32-CA9149-35]
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Interleukin-7 receptor alpha chain (IL-7R alpha) is induced upon T cell positive selection and controls thymic CD8-lineage specification and peripheral naive T cell homeostasis. How IL-7R alpha expression is regulated in developing thymocytes is unclear. Here, we show that transforming growth factor beta (TGF-beta) signaling promoted IL-7R alpha expression and CD8(+) T cell differentiation. In addition, TGF-beta signaling was required for high IL-7R alpha expression in CD4(+) T cells bearing low-affinity T cell receptors, and the abrogation of TGF-beta receptor expression led to failed maintenance of peripheral CD4(+) T cells. Compromised IL-7R alpha expression in TGF-beta-receptor-deficient T cells was associated with increased expression of the Il7ra transcriptional repressor, Gfi-1. IL-7R alpha transgenesis or T-cell-specific ablation of Gfi-1 restored IL-7R alpha expression and largely ameliorated the development and homeostasis defects of TGF-beta-receptor-deficient T cells. These findings reveal functions for TGF-beta signaling in controlling IL-7R alpha expression and in promoting T cell repertoire diversification.
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