Among these controversies, later works, however, seemed to be in favor of an atheroprotective role of pDC with a mechanism via indoleamine 2,3-dioxygenase (IDO), as pDC was demonstrated to reduce atherosclerosis by suppressing splenic CD4+T cell proliferation and activity in an IDO-dependent manner (29), and Ido1−/− atherosclerotic aorta possessed 40% fewer Treg numbers than that of WT controls, suggesting essential interaction of IDO-expressing pDCs with Tregs for the homeostasis of these cell populations in diseased aorta (85). The gene discussed is PDC; the disease is atherosclerosis.