Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF) Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Miller, A. M. Articles by Liew, F. Y. PubMed PubMed Citation Articles by Miller, A. M. Articles by Liew, F. Y. Social Bookmarking                      What's this?

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 in serum and lymph node cells. IL-33 treatment also elevated levels of total serum IgA, IgE, and IgG₁, but decreased IgG_2a, 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.

CiteULike

Complore

Connotea

Del.icio.us

Digg

Reddit

Technorati

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS