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- W4313368543 abstract "Abstract Introduction Atherosclerosis is a disease of large/medium size vessels attributed to a hyperlipidemic environment and a low-grade chronic inflammation. Normally, macrophages uptake modified low-density lipoprotein (mLDL), resulting in excess intracellular desmosterol, an immediate precursor to cholesterol, which promotes anti-inflammatory signaling. In contrast, mLDL uptake by macrophages in atherosclerosis produces foam cells that play an atherogenic role. While it has been previously shown that B cells can uptake mLDL, it remains unclear how mLDL uptake modulates B cell phenotype. Methods Murine B cells were treated with 1 mM of desmosterol for 12/24 hrs, cholesterol efflux genes were analyzed using qPCR. CFSE-labeled splenocytes were incubated with LPS/BAFF, treated with 1 mM of desmosterol for 72 hrs, and analyzed via FACS. B cells isolated from transgenic mice ooverexpressing DHCR24, a dehydrocholesterol reductase, were analyzed for desmosterol content by lipidomics, Ca2+ flux by FACS, and DNP-Ficoll induced Igs production in vivo by ELISA. Results Desmosterol uptake results in an increased expression of cholesterol efflux genes and attenuated B cell proliferation. Overexpression of DHCR24 leads to a decreased intracellular desmosterol, hyper-response of B cells shown by increased Ca2+. DNP-Ficoll immunization of B cell-deficient mice populated with either DHCR24- or WT B cells induce more anti-IGM specific Abs in the DHCR24-B cell recipients. Conclusions These results suggest desmosterol is synthesized and sensed by B cells, and its accumulation regulates B cell activation thresholds in vitro and in vivo. These novel data offer new insights for B cell biology and atherosclerosis pathology." @default.
- W4313368543 created "2023-01-06" @default.
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- W4313368543 date "2020-05-01" @default.
- W4313368543 modified "2023-09-27" @default.
- W4313368543 title "Desmosterol, an intermediate of cholesterol biosynthesis, modulates B cell activation and functions" @default.
- W4313368543 doi "https://doi.org/10.4049/jimmunol.204.supp.151.5" @default.
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