Journal
IMMUNITY
Volume 38, Issue 5, Pages 984-997Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2013.02.021
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Funding
- Leukemia and Lymphoma Society postdoctoral fellowship
- PEW charitable trust: PEW Latin American Fellow Program in Biomedical Sciences
- Howard Hughes Medical Institute
- [F32, 1F32AI096718-01A1]
- [R00 DK080885]
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Regulation of metabolic pathways in the immune system provides a mechanism to actively control cellular function, growth, proliferation, and survival. Here, we report that miR-181 is a nonredundant determinant of cellular metabolism and is essential for supporting the biosynthetic demands of early NKT cell development. As a result, miR-181-deficient mice showed a complete absence of mature NKT cells in the thymus and periphery. Mechanistically, miR-181 modulated expression of the phosphatase PTEN to control PI3K signaling, which was a primary stimulus for anabolic metabolism in immune cells. Thus miR-181-deficient mice also showed severe defects in lymphoid development and T cell homeostasis associated with impaired PI3K signaling. These results uncover miR-181 as essential for NKT cell development and establish this family of miRNAs as central regulators of PI3K signaling and global metabolic fitness during development and homeostasis.
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