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Flt3 signaling-dependent dendritic cells protect against atherosclerosis

Title
Flt3 signaling-dependent dendritic cells protect against atherosclerosis
Authors
Choi J.-H.Cheong C.Dandamudi D.Park C.Rodriguez A.Mehandru S.Velinzon K.Jung I.-H.Yoo J.-Y.Oh G.Steinman R.
Ewha Authors
오구택
SCOPUS Author ID
오구택scopus
Issue Date
2011
Journal Title
Immunity
ISSN
1074-7613JCR Link
Citation
vol. 35, no. 5, pp. 819 - 831
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Early events in atherosclerosis occur in the aortic intima and involve monocytes that become macrophages. We looked for these cells in the steady state adult mouse aorta, and surprisingly, we found a dominance of dendritic cells (DCs) in the intima. In contrast to aortic adventitial macrophages, CD11c +MHC II hi DCs were poorly phagocytic but were immune stimulatory. DCs were of two types primarily: classical Flt3-Flt3L signaling-dependent, CD103 +CD11b - DCs and macrophage-colony stimulating factor (M-CSF)-dependent, CD14 +CD11b +DC-SIGN + monocyte-derived DCs. Both types expanded during atherosclerosis. By crossing Flt3 -/- to Ldlr -/- atherosclerosis-prone mice, we developed a selective and marked deficiency of classical CD103 + aortic DCs, and they were associated with exacerbated atherosclerosis without alterations in blood lipids. Concomitantly, the Flt3 -/-Ldlr -/- mice had fewer Foxp3 + Treg cells and increased inflammatory cytokine mRNAs in the aorta. Therefore, functional DCs are dominant in normal aortic intima and, in contrast to macrophages, CD103 + classical DCs are associated with atherosclerosis protection. © 2011 Elsevier Inc.
DOI
10.1016/j.immuni.2011.09.014
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자연과학대학 > 생명과학전공 > Journal papers
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