The glucose transporter Glut1 is selectively essential for CD4 T cell activation and effector function.

Journal Article

CD4 T cell activation leads to proliferation and differentiation into effector (Teff) or regulatory (Treg) cells that mediate or control immunity. While each subset prefers distinct glycolytic or oxidative metabolic programs in vitro, requirements and mechanisms that control T cell glucose uptake and metabolism in vivo are uncertain. Despite expression of multiple glucose transporters, Glut1 deficiency selectively impaired metabolism and function of thymocytes and Teff. Resting T cells were normal until activated, when Glut1 deficiency prevented increased glucose uptake and glycolysis, growth, proliferation, and decreased Teff survival and differentiation. Importantly, Glut1 deficiency decreased Teff expansion and the ability to induce inflammatory disease in vivo. Treg cells, in contrast, were enriched in vivo and appeared functionally unaffected and able to suppress Teff, irrespective of Glut1 expression. These data show a selective in vivo requirement for Glut1 in metabolic reprogramming of CD4 T cell activation and Teff expansion and survival.

Full Text

Duke Authors

Cited Authors

  • Macintyre, AN; Gerriets, VA; Nichols, AG; Michalek, RD; Rudolph, MC; Deoliveira, D; Anderson, SM; Abel, ED; Chen, BJ; Hale, LP; Rathmell, JC

Published Date

  • July 2014

Published In

Volume / Issue

  • 20 / 1

Start / End Page

  • 61 - 72

PubMed ID

  • 24930970

Electronic International Standard Serial Number (EISSN)

  • 1932-7420

International Standard Serial Number (ISSN)

  • 1550-4131

Digital Object Identifier (DOI)

  • 10.1016/j.cmet.2014.05.004

Language

  • eng