Atherosclerosis: How the body controls the activity of Bcells
influx in response to LPI stimulation may play an important role in the regulation of cellular responses in PCs, including mitochondrial physiology and Ig productionstores, contributing to a defective BCR effector pathway activation. However, our in vitro experiments did not reveal changes in basal CaThe role of LPI in B cell GPR55 signaling and atherogenesis remains incompletely understood. In vitro, LPI stimulated B cell maturation into PCs, which was inhibited when antagonizing GPR55.
Another unresolved question remains the role of GPR55 in other immune subtypes. Our gene expression analysis of sorted splenic immune cell subsets indicates a strong GPR55 expression in T cells, which deserves further investigation in subsequent studies. The fact that GPR55 signaling in T cells is preserved may contribute to the observed differences in B cell subsets and antibody titers between the global and B-cell-specific deficiency models.
To conclude, our experimental in vivo and in vitro data, together with the confirmation of GPR55 expression and correlation with disease stage in human atherosclerosis, strongly support an implication of GPR55 in atherosclerosis. We uncovered a previously undescribed role for GPR55-LPI signaling in PC differentiation, at least in vitro.
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