Alarmins released by 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… Click to show full abstract
Alarmins released by 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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