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Updated: May 24, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
BAFF receptor deficiency reduces the development of atherosclerosis in mice--brief report
Andrew P Sage1, Dimitrios Tsiantoulas, Lauren Baker
1Division of Cardiovascular Medicine, University of Cambridge, Addenbrooke's Hospital, UK.
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.
Insights
B-cell activating factor (BAFF) receptor deficiency in mice reduces mature B2 cells, limiting atherosclerosis development. This highlights BAFF-R
Area of Science:
- Immunology
- Cardiovascular Research
- Atherosclerosis
Background:
- Atherosclerosis is a chronic inflammatory disease driven by lipid accumulation and immune responses.
- B-cell activating factor (BAFF) and its receptor (BAFF-R) play critical roles in B-cell survival and function.
- The specific role of BAFF-R in B-cell regulation of atherosclerosis remains incompletely understood.
Purpose of the Study:
- To investigate the role of BAFF receptor (BAFF-R) in B-cell mediated regulation of atherosclerosis.
- To determine how BAFF-R deficiency impacts B-cell populations and immune responses in the context of atherosclerosis.
Main Methods:
- Utilized LDL receptor-deficient (Ldlr(-/-)) mice reconstituted with wild-type or BAFF-R-deficient bone marrow.
- Mice were subjected to a high-fat diet to induce atherosclerosis.
- Analyzed B-cell subsets, dendritic cell activation, T-cell proliferation, antibody production, and atherosclerotic lesion development.
Main Results:
- BAFF-R deficiency in bone marrow cells reduced mature B2 cells but spared B1a cells.
- This reduction was associated with decreased dendritic cell activation, T-cell proliferation, and IgG antibodies against modified LDL.
- BAFF-R deficiency significantly reduced atherosclerotic lesion development and plaque T-cell infiltration.
Conclusions:
- BAFF-R deficiency in mice selectively modulates mature B2 cell-dependent immune responses.
- Targeting BAFF-R in B cells limits atherosclerotic lesion development and associated T-cell infiltration.
- These findings suggest BAFF-R as a potential therapeutic target in atherosclerosis.