%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.

@article{Goossens2010b, abstract = {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.}, added-at = {2011-03-01T12:35:22.000+0100}, author = {Goossens, P and Gijbels, M J and Zernecke, A and Eijgelaar, W and Vergouwe, M N and van der Made, I and Vanderlocht, J and Beckers, L and Buurman, W A and Daemen, M J and Kalinke, U and Weber, C and Lutgens, E and de Winther, M P}, biburl = {https://www.bibsonomy.org/bibtex/2eefe1a1e9639d22be0c23b3ad04d4d7a/kalinke}, description = {Myeloid type I interferon signaling promotes ather... [Cell Metab. 2010] - PubMed result}, doi = {10.1016/j.cmet.2010.06.008}, editor = {Oct;40(10):2769-77., Eur J Immunol. 2010}, groups = {public}, interhash = {698369d9668c4c2bc254c4b9beb093af}, intrahash = {eefe1a1e9639d22be0c23b3ad04d4d7a}, journal = {Cell Metab}, keywords = {interferon kalinke myeloid type}, month = {August}, number = 2, pages = {142-153}, pmid = {20674859}, pubmedurl = {http://www.ncbi.nlm.nih.gov/pubmed/20674859}, timestamp = {2012-05-23T13:01:55.000+0200}, title = {Myeloid type I interferon signaling promotes atherosclerosis by stimulating macrophage recruitment to lesions}, url = {http://www.ncbi.nlm.nih.gov/pubmed/20674859}, username = {kalinke}, volume = 12, year = 2010 }