%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.