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

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.

journal_name

Cell Metab

journal_title

Cell metabolism

authors

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

doi

10.1016/j.cmet.2014.05.004

subject

Has Abstract

pub_date

2014-07-01 00:00:00

pages

61-72

issue

1

eissn

1550-4131

issn

1932-7420

journal_volume

20

pub_type

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