The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20071868
The Journal of Experimental Medicine, Vol. 205, No. 2, 339-346
The Rockefeller University Press, 0022-1007 $30.00
© Miller et al.
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BRIEF DEFINITIVE REPORT

 IL-33 reduces the development of atherosclerosis

Ashley M. Miller1, Damo Xu1, Darren L. Asquith1, Laura Denby2, Yubin Li1, Naveed Sattar2, Andrew H. Baker2, Iain B. McInnes1, and Foo Y. Liew1

1 Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, and 2 British Heart Foundation Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow G12 8TA, Scotland, UK

CORRESPONDENCE Foo Y. Liew: f.y.liew{at}clinmed.gla.ac.uk OR Damo Xu: d.xu{at}clinmed.gla.ac.uk

Atherosclerosis is a chronic inflammatory disease of the vasculature commonly leading to myocardial infarction and stroke. We show that IL-33, which is a novel IL-1–like cytokine that signals via ST2, can reduce atherosclerosis development in ApoE–/– mice on a high-fat diet. IL-33 and ST2 are present in the normal and atherosclerotic vasculature of mice and humans. Although control PBS-treated mice developed severe and inflamed atherosclerotic plaques in the aortic sinus, lesion development was profoundly reduced in IL-33–treated animals. IL-33 also markedly increased levels of IL-4, -5, and -13, but decreased levels of IFN{gamma} in serum and lymph node cells. IL-33 treatment also elevated levels of total serum IgA, IgE, and IgG1, but decreased IgG2a, which is consistent with a Th1-to-Th2 switch. IL-33–treated mice also produced significantly elevated antioxidized low-density lipoprotein (ox-LDL) antibodies. Conversely, mice treated with soluble ST2, a decoy receptor that neutralizes IL-33, developed significantly larger atherosclerotic plaques in the aortic sinus of the ApoE–/– mice compared with control IgG-treated mice. Furthermore, coadministration of an anti–IL-5 mAb with IL-33 prevented the reduction in plaque size and reduced the amount of ox-LDL antibodies induced by IL-33. In conclusion, IL-33 may play a protective role in the development of atherosclerosis via the induction of IL-5 and ox-LDL antibodies.


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