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Blood, 9 April 2009, Vol. 113, No. 15, pp. 3512-3519. Prepublished online as a Blood First Edition Paper on January 7, 2009; DOI 10.1182/blood-2008-08-172767. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-08-172767v1 113/15/3512    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Caruso, R. Articles by Monteleone, G. Search for Related Content PubMed PubMed Citation Articles by Caruso, R. Articles by Monteleone, G. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Inhibition of monocyte-derived inflammatory cytokines by IL-25 occurs via p38 Map kinase–dependent induction of Socs-3 Roberta Caruso1, Carmine Stolfi1, Massimiliano Sarra1, Angelamaria Rizzo1, Massimo C. Fantini1, Francesco Pallone1, Thomas T. MacDonald2, and Giovanni Monteleone1 1 Department of Internal Medicine & Centre of Excellence for Genomic Risk Assessment in Multifactorial and Complex Diseases, University Tor Vergata of Rome, Rome, Italy; and 2 Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, United Kingdom IL-25, a member of the IL-17 cytokine family, is known to enhance Th2-like responses associated with increased serum levels of IgE, IgG1, IgA, blood eosinophilia, and eosinophilic infiltrates in various tissues. However, IL-25 also abrogates inflammatory responses driven by Th17 cells. However, the cell types that respond to IL-25 and the mechanisms by which IL-25 differentially regulates immune reactions are not well explored. To identify potential targets of IL-25, we initially examined IL-25 receptor (IL-25R) in human peripheral blood cells. IL-25R was predominantly expressed by CD14+ cells. We next assessed the functional role of IL-25 in modulating the response of CD14+ cells to various inflammatory signals. CD14+ cells responded to IL-25 by down-regulating the synthesis of inflammatory cytokines induced by toll-like receptor (TLR) ligands and inflammatory cytokines. Inhibition of cytokine response by IL-25 occurred via a p38 Map kinase–driven Socs-3–dependent mechanism. In vivo, IL-25 inhibited monocyte-derived cytokines and protected against LPS-induced lethal endotoxemia in mice. These data indicate that IL-25 is a negative regulator of monocyte proinflammatory cytokine responses, which may have therapeutic implications. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Ravoet, C. Sibille, C. Gu, M. Libin, B. Haibe-Kains, C. Sotiriou, M. Goldman, F. Roufosse, and K. Willard-Gallo Molecular profiling of CD3-CD4+ T cells from patients with the lymphocytic variant of hypereosinophilic syndrome reveals targeting of growth control pathways Blood, October 1, 2009; 114(14): 2969 - 2983. [Abstract] [Full Text] [PDF]

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