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.
Beschreibung
Myeloid type I interferon signaling promotes ather... [Cell Metab. 2010] - PubMed result
%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
}