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Role of orphan receptor GPR55 in immune cell homeostasis and atherosclerosis

Subject Area Cardiology, Angiology
Term from 2018 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 406945731
 
Final Report Year 2023

Final Report Abstract

Immune mechanisms are crucially involved in the pathogenesis of atherosclerosis and its clinical manifestations. Mounting evidence demonstrates a role of B cells and humoral immunity in atherosclerotic cardiovascular disease, which is supported by elevated titers of disease-specific antibodies (against antigens derived from modified lipoproteins, such as oxidation-specific epitopes). B cells mediate both protective and detrimental effects in cardiovascular disease, as they can secrete antibodies with both pro-atherogenic and anti-atherogenic effects. Current research efforts aim to gain an improved understanding of how B cells influence atherosclerotic disease, with the ultimate goal to develop novel B cell-targeted therapies for this life-threatening disease. In this context, we studied the immunomodulatory role of GPR55, a G-protein coupled receptor that is activated by endogenous lipid mediators. Our findings in experimental mouse models of atherosclerosis and human plaques indicate that GRP55 signaling is important for limiting B cell activation and humoral responses during hypercholesterolemia, suggesting that GPR55 signaling has an atheroprotective role.

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