Work

Mice deficient of G-protein coupled receptor 3 (GPR3) developed severe experimental autoimmune uveitis (EAU) through increased effector T cell activities

Year: 2025

Type: article

Abstract: We discovered a protective role of G protein-coupled receptor 3 (GPR3) in a mouse model of T cell-mediated autoimmune uveitis. GPR3 is an orphan receptor that maintains Gs-coupling and cyclic AMP production without an exogenous ligand. Consequently, GPR3 deficient (GPR3KO) mice were more susceptible to developing experimental autoimmune uveitis (EAU) induced by immunization with interphotoreceptor retinoid-binding protein (IRBP) or by adoptive transfer of IRBP-specific T cells than their wild type (WT) littermates. T cells isolated from IRBP-immunized GPR3KO mice demonstrated an increase in proliferation and inflammatory cytokine production in response to the specific IRBP antigen and a relatively high resistance to activation-induced T cell death compared to T cells isolated from immunized WT mice. Moreover, a major tight junction protein such as ZO-1 was reduced in GPR3 deficient retina with severe uveitis after IRBP-specific T cells were transferred. Taken together, our findings suggest that constitutively active GPR3 inhibits T cell mediated retinal inflammation.

Source: The Journal of Immunology

DOI: 10.1093/jimmun/vkaf099

Authors: Nu Chen, Jun Wu, Deming Sun, Henry J Kaplan, Hui Shao

Institutions: University of Louisville, Nanjing Medical University, University of California, Los Angeles, Doheny Eye Institute, Saint Louis University

Language: English

Topic: Ocular Diseases and Behçet’s Syndrome

Subfield: Ophthalmology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: hybrid

Estimated APC paid: $3,500