GPR132 regulates CD8⁺ T cell responses to infection

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Presentation Time: 11:30 AM - 12:45 PM
Poster Board Number: B617
Abstract ID: 5824

Presenting Author:
Giuseppina Marchesini Tovar , Predoctoral Fellow at Rutgers New Jersey Med. Sch., Rutgers School of Graduate Studies

Abstract:

CD8+ T cells undergo robust expansion upon priming; however, T cell function must be tightly regulated to ensure effective immunosurveillance without immunopathology. G protein coupled receptors sense environmental signals and are essential for modulating T cell function. GPR132 recognizes oxidized fatty acids generated by the host during inflammation and commensal bacteria, and Gpr132KO mice develop autoimmunity accompanied by expansion of the T cell compartment. T cells express GPR132 early after activation and into the memory phase, implicating GPR132 as a key target for their regulation. We examined the role of GPR132 in T cell responses to diverse stimuli. After TCR-engagement in vitro, wildtype (WT) and KO T cells had similar proliferation and gene expression profiles. Similar results were observed during lymphopenia-driven proliferation in vivo. However, after infection, KO T cells displayed 3-4 fold increased expansion over WT cells in all tissues, indicating GPR132 inhibits T cell expansion specifically in this context. Further examination of the interplay of TCR and GPR132 signaling revealed a more prominent role for GPR132 during high affinity TCR stimulation in vivo. GPR132 also regulates effector function, and granzyme production was reduced in KO compared to WT T cells. These studies reveal a role for GPR132-mediated detection of self and commensal lipids in regulating T cell responses to pathogens and indicate GPR132 can be targeted to modulate T cell function.