期刊
CELL METABOLISM
卷 12, 期 2, 页码 142-153出版社
CELL PRESS
DOI: 10.1016/j.cmet.2010.06.008
关键词
-
资金
- Netherlands Heart Foundation [2005B175, 2007T067, 2009T034]
- Netherlands Organization [917-66-329, 016-086-326]
- European Union [MEST-CT-2005-020706/CADRE2]
- Humboldt foundation
- European Vascular Genomics Network (EVGN)
Inflammatory cytokines are well-recognized mediators of atherosclerosis. Depending on the pathological context, type I interferons (IFNs; IFN alpha and IFN beta) exert either pro- or anti-inflammatory immune functions, but their exact role in atherogenesis has not been clarified. Here, we demonstrate that IFN beta enhances macrophage-endothelial cell adhesion and promotes leukocyte attraction to atherosclerosis-prone sites in mice in a chemokine-dependent manner. Moreover, IFN beta treatment accelerates lesion formation in two different mouse models of atherosclerosis and increases macrophage accumulation in the plaques. Concomitantly, absence of endogenous type I IFN signaling in myeloid cells inhibits lesion development, protects against lesional accumulation of macrophages, and prevents necrotic core formation. Finally, we show that type I IFN signaling is upregulated in ruptured human atherosclerotic plaques. Hereby, we identify type I IFNs as proatherosclerotic cytokines that may serve as additional targets for prevention or treatment.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据