The glucose transporter Glut1 is selectively essential for CD4 T cell activation
and effector function.
Authors Macintyre AN, Gerriets VA, Nichols AG, Michalek RD, Rudolph MC, Deoliveira D,
Anderson SM, Abel ED, Chen BJ, Hale LP, Rathmell JC
Submitted By Submitted Externally on 3/4/2015
Status Published
Journal Cell Metabolism
Year 2014
Date Published 7/1/2014
Volume : Pages 20 : 61 - 72
PubMed Reference 24930970
Abstract 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.

Investigators with authorship
E. Dale AbelUniversity of Iowa