Functional heterogeneity of dendritic cells (DCs) observed in atherosclerosis suggest for their complex and multifaced role in the pathogenesis of atherosclerotic disease. A delicate balance between anti-inflammatory and pro-inflammatory mechanisms drives atherogenesis, and local microenvironment triggers the actual involvement of DCs in atherosclerosis-associated inflammation. Responding to microenvironment stimuli, DCs contribute to atherogenesis in both ways being involved in supporting proatherogenic vascular inflammation and by suppressing inflammatory responses via induction of self-tolerogenic properties and regulatory T cells (Tregs). The local microenvironment and extrinsic stimuli influence DC phenotype and hence could control the phenotypic switch toward inflammation or tolerance.