Abstract
Dendritic cells (DCs), as a bridge between innate and adaptive immunity, play key roles in atherogenesis, particularly in plaque rupture, the underlying pathophysiologic cause of myocardial infarction. Targeting DC functions, including maturation and migration to atherosclerotic plaques, may be a novel therapeutic approach to atherosclerotic disease. Dimethyl fumarate (DMF), an agent consisting of a combination of fumaric acid esters, in current study were found to be able to suppress DC maturation by reducing the expression of costimulatory molecules and MHC class II and by blocking cytokine secretion. In addition, DMF efficiently inhibited the migration of activated DCs in vitro and in vivo by reducing the expression of chemokine receptor 7 (CCR7). Additionally, DMF efficiently inhibited the expression of the costimulatory molecule CD86, as well as the chemokine receptor CCR7 and the C-X-C motif chemokine receptor 4 (CXCR4), in healthy donor-derived purified DCs that had been stimulated by ST-segment elevation myocardial infarction (STEMI) patient serum. This study points to the potent therapeutic value of DMF for protecting against cardiovascular disease by suppressing DC functions.
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