%0 Journal Article %1 Goossens2010b %A Goossens, P %A Gijbels, M J %A Zernecke, A %A Eijgelaar, W %A Vergouwe, M N %A van der Made, I %A Vanderlocht, J %A Beckers, L %A Buurman, W A %A Daemen, M J %A Kalinke, U %A Weber, C %A Lutgens, E %A de Winther, M P %D 2010 %E Oct;40(10):2769-77., Eur J Immunol. 2010 %J Cell Metab %K interferon kalinke myeloid type %N 2 %P 142-153 %R 10.1016/j.cmet.2010.06.008 %T Myeloid type I interferon signaling promotes atherosclerosis by stimulating macrophage recruitment to lesions %U http://www.ncbi.nlm.nih.gov/pubmed/20674859 %V 12 %X Inflammatory cytokines are well-recognized mediators of atherosclerosis. Depending on the pathological context, type I interferons (IFNs; IFNalpha and IFNbeta) exert either pro- or anti-inflammatory immune functions, but their exact role in atherogenesis has not been clarified. Here, we demonstrate that IFNbeta enhances macrophage-endothelial cell adhesion and promotes leukocyte attraction to atherosclerosis-prone sites in mice in a chemokine-dependent manner. Moreover, IFNbeta 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.