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Cardiovascular Research Advance Access first published online on May 16, 2008
This version [Corrected Proof] published online on June 9, 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*, Susanne Zadelaar and Teake Kooistra

TNO-BioSciences, Gaubius-Laboratory, Department of Vascular and Metabolic Diseases, PO Box 2215, 2301 CE Leiden, The Netherlands

* Corresponding author. Tel: +31 71 518 1467; fax: +31 71 518 1901. E-mail address: 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 [tumour 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, and disease stage). An important outcome of this survey is (i) 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}, and M-CSF) or antiatherogenic (IL-10) and (ii) 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.

KEYWORDS Atherosclerosis; Inflammation; Cytokines; Interleukins; Macrophage

Time for primary review: 19 days


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