Due to their vital functions, the wall structures of arteries are immunoprivileged sites and protected from autoimmune destruction. However, such chronic inflammation as atheroselerosis and vasculitis have frequently been reported in aortie tissues, where phagocytic immune cells play important roles via innate or adaptive immunity. Unfortunately, the limited cellularity of the vasculatures makes the study of aortic regional immune cells difficult, and thus their links to aortic inflammation remain inconclusive. Previously,we reported that healthy aortic tissues have unique double edged immunological features to explain the pathophysiology of aorta. Here in the diseased animals with unaltered immune system, we found that the proportion ofaortic DCs, especially moDC subset increased significantlyand aortic,not splenicT cells have a distinet pro-inflammatory phenotype, concomitant with the activated status of aortic antigen presenting cells. Further experiment revealed that aortic DCs, but not Mφ or B cells, elevated both model and cognate antigen presentation to stimulate local T cells during atherosclerosis, in which cDC1 subset demonstrated the best capacity to activate both CD4⁺ and CD8⁺T cells.Interestingly aortic moDCs were found to be the major source of IL-12 for Th1 differentiation in atherosclerotic aorta.Finally, immunization of pro-atheroselerotic mice with OVA antigen presented byaortic DCs led to early onset ofatherosclerotic plaque and atherosclerosis-like aortic inflammation. Together, we provided direct evidences for the adaptive immunological functions of aortic DCs in atherogenesis with differential pathogenic roles at subset levels, which could have serious implication in understanding and targeted treatment of cardiovascular autoinflammation.