期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 207, 期 8, 页码 1579-1587出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20100155
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资金
- Institut National de la Sante et de la Recherche Medicale
- transatlantic Leducq Immunoregulatory Network
- European Union
- Fund of Scientific Medical Research
- Belgian Federal Service for Scientific, Technical, and Cultural Affairs
- National Institutes of Health [CA105001, AI56363, AI057157]
- British Heart Foundation [RG/10/001/27643] Funding Source: researchfish
B cell depletion significantly reduces the burden of several immune-mediated diseases. However, B cell activation has been until now associated with a protection against atherosclerosis, suggesting that B cell-depleting therapies would enhance cardiovascular risk. We unexpectedly show that mature B cell depletion using a CD20-specific monoclonal antibody induces a significant reduction of atherosclerosis in various mouse models of the disease. This treatment preserves the production of natural and potentially protective anti-oxidized low-density lipoprotein (oxLDL) IgM autoantibodies over IgG type anti-oxLDL antibodies, and markedly reduces pathogenic T cell activation. B cell depletion diminished T cell-derived IFN-gamma secretion and enhanced production of IL-17; neutralization of the latter abrogated CD20 antibody-mediated atheroprotection. These results challenge the current paradigm that B cell activation plays an overall protective role in atherogenesis and identify new antiatherogenic strategies based on B cell modulation.
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