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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 (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 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. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 7, 2008 Accepted December 5, 2008 Inhibition of monocyte-derived inflammatory cytokines by IL-25 occurs via a p38 Map kinase-dependent induction of SOCS-3 Roberta Caruso, Carmine Stolfi, Massimiliano Sarra, Angelamaria Rizzo, Massimo Claudio Fantini, Francesco Pallone, Thomas T MacDonald, and Giovanni Monteleone* Department of Internal Medicine, University "Tor Vergata" of Rome, Rome, Italy Institute of Cell and Molecular Science, Bart's and the London School of Medicine and Dentistry, London, United Kingdom * Corresponding author; email: gi.monteleone{at}med.uniroma2.it. 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. On the other hand, 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 pro-inflammatory 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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