| First Author | Sage AP | Year | 2012 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 32 |
| Issue | 7 | Pages | 1573-6 |
| PubMed ID | 22426131 | Mgi Jnum | J:201505 |
| Mgi Id | MGI:5514225 | Doi | 10.1161/ATVBAHA.111.244731 |
| Citation | Sage AP, et al. (2012) BAFF receptor deficiency reduces the development of atherosclerosis in mice--brief report. Arterioscler Thromb Vasc Biol 32(7):1573-6 |
| abstractText | 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. |
