Atherosclerosis is characterized by the deposition of lipids in the arterial wall, along with the infiltration of macrophages, dendritic cells (DCs, derived from the Greek word “dendron,” meaning tree), and T cells, which are involved in both innate and adaptive immunity. Among these, DCs are the most professional antigen-presenting cells, surpassing macrophages. DCs capture diverse antigens, present them to T cells, and induce immune responses. Depending on the situation, DCs can also inhibit T cell activation (Steinman 2007; Steinman and Banchereau 2007; Granucci et al. 2008; Bobryshev 2010). The ability of DCs to activate or inhibit T cells depends on their cytokine production and the expression of co-stimulatory molecules on their cell surface. When activated by innate immune receptors such as Toll-like receptors (TLRs), DCs become potent antigen-presenting cells, presenting antigens to naive, memory, and effector T cells, and activating them. In the absence of activation, DCs do not express co-stimulatory molecules, and their antigen presentation to T cells leads to immunological tolerance (Blanco et al. 2008). Therefore, DCs play a crucial role in bridging innate and adaptive immunity.