Colloquia

  • Vascular Immune Cell Network in the Pathogenesis of Atherosclerosis

  • Speaker : Goo Taeg Oh
    Affiliation : Ewha Womans University
    Date : 09/06/2016 4:00 pm
    Place : Engineering Building E104
    Contact : kjk10410@unist.ac.kr
  • Abstract

  • Atherosclerosis is a chronic inflammatory disease that intense immunological pathways play an essential role. During the progression of atherosclerosis, large numbers of inflammatory and immune cells accumulate in intima. The accumulated immune cells, including T cells, macrophages, and dendritic cells (DCs), cross-talk each other, and affect the development of atherosclerosis. Importantly, we found DCs that were poorly phagocytic but were immune stimulatory in the steady state mouse aorta. By crossing Flt3-/- to Ldlr-/- mice, deficiency of classical CD103+ aortic DCs exacerbated atherosclerosis and fewer Foxp3+ Treg cells. These data indicate that functional DCs are dominant in normal aortic intima, and CD103+ classical DCs are associated with atherosclerosis protection. The function of CD137, a member of the tumor necrosis factor receptor superfamily, in mediating atherosclerosis plaque stability remains unknown. We found that activation of CD137 signaling decreases the stability of plaques via its combined effects on T cells, vascular smooth muscle cells, and macrophages. Recently, we found that anti-oxidant Peroxiredoxin 1 (Prdx1) is crucial to regulating lipophagic flux and maintain macrophage cholesterol homeostasis against oxidative stress.