Print Email Facebook Twitter Cytokines and atherosclerosis: A comprehensive review of studies in mice Title Cytokines and atherosclerosis: A comprehensive review of studies in mice Author Kleemann, R. Zadelaar, A.S.M. Kooistra, T. Gaubius Instituut TNO Publication year 2008 Abstract 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-α (TNF-α); macrophage migration inhibitory factor (MIF); interferon-γ (IFN-γ); 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-γ, TNF-α, 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. © The Author 2008. Chemicals / CAS: colony stimulating factor 1, 81627-83-0; gamma interferon, 82115-62-6; interleukin 12, 138415-13-1; interleukin 18, 189304-55-0; interleukin 2, 85898-30-2; Colony-Stimulating Factors; Cytokines; Interferon-gamma, 82115-62-6; Interleukins; Macrophage Migration-Inhibitory Factors; Tumor Necrosis Factor-alpha Subject HealthAtherosclerosisCytokinesMacrophageGamma interferonGranulocyte colony stimulating factorGranulocyte macrophage colony stimulating factorInterleukin 1Interleukin 10Interleukin 12Interleukin 18Interleukin 2Interleukin 20Interleukin 3Interleukin 4Interleukin 5Interleukin 6AtherogenesisDietGene deletionGene overexpressionMouse strainNonhumanOutcome assessmentProtein expressionReviewSex differenceAnimalsAtherosclerosisColony-Stimulating FactorsCytokinesDisease Models, AnimalInflammationInterferon-gammaInterleukinsMacrophage Migration-Inhibitory FactorsMiceSignal TransductionTumor Necrosis Factor-alpha To reference this document use: http://resolver.tudelft.nl/uuid:5c705240-e889-432a-98c9-0552adf86392 DOI https://doi.org/10.1093/cvr/cvn120 TNO identifier 240929 ISSN 0008-6363 Source Cardiovascular Research, 79 (3), 360-376 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.