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Cardiovascular Research Advance Access [Accepted Manuscript] published online on May 16, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn120
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Cytokines and atherosclerosis: a comprehensive review of studies in mice

Robert Kleemann, PhD, Susanne Zadelaar, PhD and Teake Kooistra, PhD

TNO-BioSciences, Gaubius-Laboratory, Department of Vascular and Metabolic Diseases, Leiden, The Netherlands

Corresponding author: Robert Kleemann, PhD TNO-BioSciences P.O.Box 2215 2301-CE-Leiden The Netherlands T: +31-71-518-1467 F: +31-71-518-1901 E-mail: Robert.Kleemann{at}tno.nl

In the past few years, inflammation has emerged as a major driving force of atherosclerotic lesion development. It is now well-established that from early lesion to vulnerable plaque formation numerous cellular and molecular inflammatory components participate in the disease process. The most prominent cells that invade in evolving lesions are monocyte-derived macrophages and T-lymphocytes. Both cell types produce a wide array of soluble inflammatory mediators (cytokines, chemokines) which are critically important in the initiation and perpetuation of the disease.

This review summarizes the currently available information from mouse studies on the contribution of a specified group of cytokines expressed in atherosclerotic lesions, viz. interleukins (IL-1,-IL-2,-IL-3,-IL-4,-IL-5,-IL-6,-IL-10,-IL-12,-IL-18,-IL-20) and macrophage-associated cytokines (tumor necrosis factor-{alpha} (TNF-{alpha}); macrophage migration inhibitory factor (MIF); interferon-{gamma} (IFN-{gamma}); colony stimulating factors G-CSF,-M-CSF,-GM-CSF) to atherogenesis. Emphasis is put on the consistency of the effects of these cytokines, i.e. inasmuch an effect depends on the experimental approach applied (overexpression/deletion, strain, gender, dietary conditions, disease stage). An important outcome of this survey is a) that only for a few cytokines there is sufficient consistent data allowing classifying them as typically proatherogenic (IL-1, IL-12, IL-18, MIF, IFN{gamma}, TNF-{alpha}, M-CSF) or antiatherogenic (IL-10) and b) that some cytokines (IL-4, IL-6 and GM-CSF) can exert pro- or anti-atherogenic effects depending on the experimental conditions. This knowledge can be used for improved early detection, prevention and treatment of atherosclerosis.

Time for primary review: 19 days


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