Flt3 Signaling-Dependent Dendritic Cells Protect against Atherosclerosis
作者： Jae-Hoon Choi , Cheolho Cheong , Durga B. Dandamudi , Chae Gyu Park , Anthony Rodriguez
DOI: 10.1016/J.IMMUNI.2011.09.014
关键词:
摘要: Early events in atherosclerosis occur the aortic intima and involve monocytes that become macrophages. We looked for these cells steady state adult mouse aorta, surprisingly, we found a dominance of dendritic (DCs) intima. In contrast to adventitial macrophages, CD11c(+)MHC II(hi) DCs were poorly phagocytic but immune stimulatory. two types primarily: classical Flt3-Flt3L signaling-dependent, CD103(+)CD11b(-) macrophage-colony stimulating factor (M-CSF)-dependent, CD14(+)CD11b(+)DC-SIGN(+) monocyte-derived DCs. Both expanded during atherosclerosis. By crossing Flt3(-/-) Ldlr(-/-) atherosclerosis-prone mice, developed selective marked deficiency CD103(+) DCs, they associated with exacerbated without alterations blood lipids. Concomitantly, Flt3(-/-)Ldlr(-/-) mice had fewer Foxp3(+) Treg increased inflammatory cytokine mRNAs aorta. Therefore, functional are dominant normal and, protection.
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