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Background: B1a and B1b lymphocytes produce IgM that inactivates oxidation-specific epitopes (IgM) on LDL (low-density lipoprotein) and protects against atherosclerosis. Loss of ID3 (inhibitor of differentiation 3) in B cells selectively promotes B1b but not B1a cell numbers, leading to higher IgM production and reduction in atherosclerotic plaque formation. Yet, the mechanism underlying this regulation remains unexplored.
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