BAFF receptor deficiency reduces the development of atherosclerosis in mice--brief report.

Change log
Sage, Andrew P 
Tsiantoulas, Dimitrios 
Baker, Lauren 
Masters, Leanne 

OBJECTIVE: The goal of this study was to assess the role of B-cell activating factor (BAFF) receptor in B-cell regulation of atherosclerosis. METHODS AND RESULTS: Male LDL receptor-deficient mice (Ldlr(-/-)) were lethally irradiated and reconstituted with either wild type or BAFF receptor (BAFF-R)-deficient bone marrow. After 4 weeks of recovery, mice were put on a high-fat diet for 6 or 8 weeks. BAFF-R deficiency in bone marrow cells led to a marked reduction of conventional mature B2 cells but did not affect the B1a cell subtype. This was associated with a significant reduction of dendritic cell activation and T-cell proliferation along with a reduction of IgG antibodies against malondialdehyde-modified low-density lipoprotein. In contrast, serum IgM type antibodies were preserved. Interestingly, BAFF-R deficiency was associated with a significant reduction in atherosclerotic lesion development and reduced numbers of plaque T cells. Selective BAFF-R deficiency on B cells led to a similar reduction in lesion size and T-cell infiltration but in contrast did not affect dendritic cell activation. CONCLUSIONS: BAFF-R deficiency in mice selectively alters mature B2 cell-dependent cellular and humoral immune responses and limits the development of atherosclerosis.

Animals, Atherosclerosis, B-Cell Activation Factor Receptor, Lymphocyte Activation, Male, Mice, Mice, Inbred C57BL, T-Lymphocytes
Journal Title
Arterioscler Thromb Vasc Biol
Conference Name
Journal ISSN
Volume Title
Ovid Technologies (Wolters Kluwer Health)
British Heart Foundation (None)
British Heart Foundation, Fondation Leducq.