
B cells have an important role in exacerbating the progression of established atherosclerosis after myocardial infarction (MI). According to a new study, alarmins released by the infarcted myocardium stimulate B cells to differentiate into antibody-producing plasma cells, which then remotely drive the progression of atherosclerosis by producing autoantibodies that accumulate in pre-existing atherosclerotic plaques, increasing local inflammation and accelerating the progression towards a vulnerable plaque phenotype.
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