Title : Glucose uptake is limiting in T cell activation and requires CD28-mediated Akt-dependent and independent pathways.

Pub. Date : 2008 Apr 1

PMID : 18354169






6 Functional Relationships(s)
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1 We show that glucose uptake is limiting in T cell activation and that CD28 costimulation is required to allow maximal glucose uptake following TCR stimulation by up-regulating expression and promoting the cell surface trafficking of the glucose transporter Glut1. Glucose solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus
2 We show that glucose uptake is limiting in T cell activation and that CD28 costimulation is required to allow maximal glucose uptake following TCR stimulation by up-regulating expression and promoting the cell surface trafficking of the glucose transporter Glut1. Glucose solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus
3 Regulation of T cell glucose uptake and Glut1 was critical, as low glucose prevented appropriate T cell responses. Glucose solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus
4 In support of this model, coexpression of Glut1 and myristoylated Akt transgenes resulted in a synergistic increase in glucose uptake and accumulation of activated T cells in vivo that were largely independent of CD28. Glucose solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus
5 Induction of Glut1 protein and Akt regulation of Glut1 trafficking are therefore separable functions of CD28 costimulation that cooperate to promote glucose metabolism for T cell activation and proliferation. Glucose solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus
6 Induction of Glut1 protein and Akt regulation of Glut1 trafficking are therefore separable functions of CD28 costimulation that cooperate to promote glucose metabolism for T cell activation and proliferation. Glucose solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus