Abstract
Abstract GPR65 has been shown to be a critical regulator of Th17 pathogenicity. Loss of GPR65 in mice results in a decrease in Th17 cells and reduced susceptibility to experimental autoimmune encephalomyelitis. 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 Th17 cells. In this study we performed RNA-seq to identify Th17 genes regulated by the CREB/CRTC2 pathway. Our RNA-seq analysis led us to uncover the first mechanism of regulation of the orphan receptor GPR65 by the CREB/CRTC2 pathway. We show that GPR65 is a target of the CREB/CRTC2 pathway through expression studies and chromatin immunoprecipitation. In addition, we show that targeting of GPR65 with small molecules alters Th17 cell differentiation. Understanding the regulation of GPR65 will be crucial in developing small molecules to treat patients with Th17-mediated diseases.
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