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G-protein-coupled receptor P2Y10 facilitates chemokine-induced CD4 T cell migration through an autocrine feedback loop involving ATP and lysophosphatidylserine

ABSTRACT: G-Protein-coupled receptors (GPCRs), especially chemokine receptors, play a central role in the regulation of T cell migration. Various GPCRs are upregulated in activated CD4 T cells, among them P2Y10, a putative lysophospholipid receptor that is officially still considered an orphan GPCR. P2Y10-deficient CD4 T cells showed normal activation, differentiation, and proliferation, but reduced chemokine-induced migration and polarization. Chemokine-induced activation of RhoA, a central regulator of polarization and migration, was reduced in the absence of P2Y10, and this was due to loss of an autocrine feedback loop involving chemokine-triggered release of lysophosphatidylserine and adenosine triphosphate and consecutive P2Y10-dependent RhoA activation. In line with impaired chemokine-induced T cell migration, we found that mice with CD4 T cell-specific P2Y10 deficiency showed reduced T cell infiltration into the spinal cord in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis

ORGANISM(S): Mus musculus

PROVIDER: GSE162246 | GEO | 2021/09/21

REPOSITORIES: GEO

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G-protein-coupled receptor P2Y10 facilitates chemokine-induced CD4 T cell migration through an autocrine feedback loop involving ATP and lysophosphatidylserine

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