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GPR55 in B cells limits atherosclerosis development and regulates plasma cell maturation.
- Source :
-
Nature cardiovascular research [Nat Cardiovasc Res] 2022 Nov; Vol. 1, pp. 1056-1071. Date of Electronic Publication: 2022 Nov 11. - Publication Year :
- 2022
-
Abstract
- 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 (PC), 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 immunoglobulin (Ig)G 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.<br />Competing Interests: Competing interests The authors declare no conflicts of interests.
Details
- Language :
- English
- ISSN :
- 2731-0590
- Volume :
- 1
- Database :
- MEDLINE
- Journal :
- Nature cardiovascular research
- Publication Type :
- Academic Journal
- Accession number :
- 36523570
- Full Text :
- https://doi.org/10.1038/s44161-022-00155-0