In contrast, mature DCs are obviously increased in atherosclerosis plaques, mediating antigen presentation, the production of costimulation (CD80/CD86), and pro-inflammatory cytokine [IL-6, interferon-γ (IFN-γ), etc.] in the inflammatory immune microenvironment, which trigger T cell overproliferation and differentiation and exacerbate atherosclerosis eventually [18]. The gene discussed is CD86; the disease is atherosclerosis.