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- W4313382013 abstract "Abstract Atherosclerosis is a multifaceted chronic inflammatory disease characterized by the accumulation of modified lipoproteins and immune cells in the aortic wall and vascular dysfunction. The uptake of modified low density lipoproteins (mLDL) by MFs plays an important role in atherosclerosis through the modulation of cholesterol metabolism and MF activation. To date, the impact of mLDL on B cell phenotype and functions is unaddressed. We show that B cells can uptake acetylated and oxidized LDL (acLDL and oxLDL, respectively) via a dynamin-dependent pathway in a concentration, time, and temperature-dependent manner. Assessment of the transcriptional profiles of in vivo acLDL+ B cells and acLDL- B cells by RNAseq suggests that acLDL+ B cells assume an anergic like phenotype. Anergy plays an important role in keeping autoreactive B cells in a state of unresponsiveness and the loss of anergy contributes to the development of autoimmune diseases. Currently, nothing is known about the role and regulation of B cell anergy in atherosclerosis. We show here for the first time that GRAIL, an E3 ubiquitin ligase associated with T cell tolerance, is expressed in B cells. To determine whether B cell-specific GRAIL expression plays a role in atherosclerosis, we performed adoptive transfer of GRAIL-deficient or GRAIL-sufficient B cells into B-cell-deficient mice on apolipoprotein-E deficient background (uM−/− Apoe−/−) mice and examined atherogenesis after 8 weeks of western diet feeding. B cell-specific GRAIL-deficiency supported plaque burden and orchestrated inflammation in the aortic wall. These data suggest that there is a specific mechanism by which B cells recognize mLDL and regulate their anergy-dependent response to mLDL in atherosclerosis." @default.
- W4313382013 created "2023-01-06" @default.
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- W4313382013 date "2017-05-01" @default.
- W4313382013 modified "2023-09-27" @default.
- W4313382013 title "Modified low density lipoprotein (mLDL) uptake by B cells alters B cell phenotype and impacts atherosclerosis." @default.
- W4313382013 doi "https://doi.org/10.4049/jimmunol.198.supp.220.16" @default.
- W4313382013 hasPublicationYear "2017" @default.
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