Scientific article
Open access

GPR55 in B cells limits atherosclerosis development and regulates plasma cell maturation

Published inNature cardiovascular research, vol. 1, no. 11, p. 1056-1071
Publication date2022-11-11
First online date2022-11-11

Dissecting the pathways regulating the adaptive immune response in atherosclerosis is of particular therapeutic interest. Here we report that the lipid G-protein-coupled receptor GPR55 is highly expressed by splenic plasma cells (PCs), upregulated in mouse spleens during atherogenesis and human unstable or ruptured compared to stable plaques. Gpr55 -deficient mice developed larger atherosclerotic plaques with increased necrotic core size compared to their corresponding controls. Lack of GPR55 hyperactivated B cells, disturbed PC maturation and resulted in IgG overproduction. B-cell-specific Gpr55 depletion or adoptive transfer of Gpr55 -deficient B cells was sufficient to promote plaque development and elevated IgG titers. In vitro, the endogenous GPR55 ligand lysophsophatidylinositol (LPI) enhanced PC proliferation, whereas GPR55 antagonism blocked PC maturation and increased their mitochondrial content. Collectively, these discoveries provide previously undefined evidence for GPR55 in B cells as a key modulator of the adaptive immune response in atherosclerosis.

Citation (ISO format)
GUILLAMAT-PRATS, Raquel et al. GPR55 in B cells limits atherosclerosis development and regulates plasma cell maturation. In: Nature cardiovascular research, 2022, vol. 1, n° 11, p. 1056–1071. doi: 10.1038/s44161-022-00155-0
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ISSN of the journal2731-0590

Technical informations

Creation11/21/2022 9:03:00 AM
First validation11/21/2022 9:03:00 AM
Update time03/16/2023 10:54:55 AM
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