Article

CREB/CRTC2-Induced GPR65 Orchestrates Th17 Metabolic Fitness and Pathogenic Effector Function

2026-03-30

Abstract excerpt

<h4>ABSTRACT</h4> GPR65 has been shown to be a critical regulator of Th17 cell pathogenicity. Loss of GPR65 in mice results in a decrease in Th17 cells and reduced susceptibility to a mouse model of multiple sclerosis. The CREB/CRTC2 pathway has emerged as an important regulator of immune function. We have previously shown that the CREB/CRTC2 pathway modulates autoimmune disease by promoting differentiation of Th...

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Literature Corpus work: 7d903777-c5df-585f-85b2-a31b2229d04f
DOI: 10.64898/2026.03.27.714848

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