Abstract
[Figure: see text].
Highlights
Using hypercholesterolemic apolipoprotein-E deficient mice, we demonstrate that whole-body CD200 deficiency augments atherosclerotic lesion formation and vulnerability
Innate immunity is a key component of atherosclerosis, the main cause of cardiovascular disease (CVD)
Expression of CD200 and CD200R during atherogenesis was assessed in aortic roots of chow-fed apolipoprotein E-deficient (ApoE−/−) mice aged 12, 20, and 28 weeks
Summary
Using hypercholesterolemic apolipoprotein-E deficient mice, we demonstrate that whole-body CD200 deficiency augments atherosclerotic lesion formation and vulnerability. Our data show that the CD200-CD200R pathway restrains activation of CD200R+ lesional macrophages, their production of CCR2 ligands, and monocyte recruitment in vitro and in vivo in an air pouch model. Loss of CD200 leads to an excessive accumulation of classical Ly6Chi monocytes and CCR2+ macrophages within the atherosclerotic aorta, as assessed by mass cytometry. We uncover a previously uncharacterized effect of the CD200/CD200R pathway in limiting dysregulated monopoiesis and Ly6Chi monocytosis in hypercholesterolemic mice. Bone marrow chimera experiments demonstrate that the CD200-CD20R pathway enables 2 complementary and tissue-dependent strategies to limit atherogenesis: CD200 expression by bone marrow–derived cells limits systemic monocytosis, while CD200 expression by nonhematopoietic cells, for example, endothelial cells, prevents local plaque growth. CD200R expression on classical monocytes in peripheral blood of patients with coronary artery disease is associated with a lower burden of coronary artery disease and a more favorable Virtual Histology plaque profile
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