|| Checking for direct PDF access through Ovid
Inflammation, in addition to high cholesterol is a major factor contributing to atherosclerosis-associated adverse cardiovascular events. Thus, there is a pressing need for additional therapeutic strategies to reduce inflammation, by targeting immune cells and cytokines. Here we review B cell subsets and adventitial and intimal B cells in atherosclerosis development and discuss potential B cell-targeted anti-inflammatory therapies for atherosclerosis.B cell subsets can have opposing proatherogenic and atheroprotective roles in atherosclerosis. CD-20-targeted B cell depletion has been shown to decrease murine atherosclerotic lesions. The accumulation of intimal and adventitial B cells associated with atherosclerotic lesions is consistent with their participation in local inflammatory responses. As B2 B cells are proatherogenic, blocking its survival factor B cell activating factor may selectively delete this proatherogenic subset.Both intimal and adventitial B cells appear important in atherosclerosis. B2 B cells are proatherogenic and other subsets such as regulatory B cells are antiatherogenic. Future B cell-targeted therapy for atherosclerosis should be customized to selectively deplete damaging B2 B cells while sparing or expanding protective B cell subsets.