Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 97, Issue 2, Pages 279-283Publisher
FEDERATION AMER SOC EXP BIOL
DOI: 10.1189/jlb.2AB0514-273RR
Keywords
signal transduction; metabolism; lymphocyte; autoimmunity
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Funding
- Intramural Program of National Institute of Allergy and Infectious Diseases (NIAID), U.S. National Institutes of Health
- Cooperative Research and Development Agreement (CRADA)
- Boerhinger-Ingelheim
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CD4(+)CD25(+)Foxp3(+)T(regs) have a diminished capacity to activate the PI3K/Akt pathway. Although blunted Akt activity is necessary to maintain T-reg function, the consequences of this altered signaling are unclear. Glut1 is a cell-surface receptor responsible for facilitating glucose transport across plasma membranes, whose expression is tightly coupled to costimulatory signals and Akt phosphorylation. Freshly isolated human T-regs were unable to up-regulate Glut1 in response to TCR and costimulatory signals compared with T-conv. Consequently, the ability of T-regs to use glucose was also reduced. Introduction of Foxp3 into T-conv inhibited Akt activation and Glut1 expression, indicating that Foxp3 can regulate Glut1. Finally, pharmacologic activation of Akt in T-regs can induce Glut1, overcoming the effects of Foxp3. Together, these results illustrate the molecular basis behind differential glucose metabolism in T-regs.
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