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Prepublished online as a Blood First Edition Paper on September 12, 2002; DOI 10.1182/blood-2002-02-0538. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-02-0538v1 101/2/729    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 Berrebi, D. Articles by Emilie, D. Search for Related Content PubMed PubMed Citation Articles by Berrebi, D. Articles by Emilie, D. Related Collections Immunobiology Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 January 2003, Vol. 101, No. 2, pp. 729-738 PHAGOCYTES Synthesis of glucocorticoid-induced leucine zipper (GILZ) by macrophages: an anti-inflammatory and immunosuppressive mechanism shared by glucocorticoids and IL-10 Dominique Berrebi, Stefano Bruscoli, Nicolas Cohen, Arnaud Foussat, Graziella Migliorati, Laurence Bouchet-Delbos, Marie-Christine Maillot, Alain Portier, Jacques Couderc, Pierre Galanaud, Michel Peuchmaur, Carlo Riccardi, and Dominique Emilie From the Institut National de la Santé et de la Recherche Médicale (INSERM) U131, Institut Paris-Sud sur les Cytokines, Clamart, France; Service d'Anatomie et de Cytologie Pathologiques, Equipe d'Accueil 3102 (UPRESA 3102), Hôpital Robert Debré, Paris, France; and the Department of Clinical and Experimental Medicine, Section of Pharmacology, University of Perugia, Via del Giochetto, Perugia, Italy. Glucocorticoids and interleukin 10 (IL-10) prevent macrophage activation. In murine lymphocytes, glucocorticoids induce expression of glucocorticoid-induced leucine zipper (GILZ), which prevents the nuclear factor B (NF-B)-mediated activation of transcription. We investigated whether GILZ could account for the deactivation of macrophages by glucocorticoids and IL-10. We found that GILZ was constitutively produced by macrophages in nonlymphoid tissues of humans and mice. Glucocorticoids and IL-10 stimulated the production of GILZ by macrophages both in vitro and in vivo. Transfection of the macrophagelike cell line THP-1 with the GILZ gene inhibited the expression of CD80 and CD86 and the production of the proinflammatory chemokines regulated on activation normal T-cell expressed and secreted (CCL5) and macrophage inflammatory protein 1 (CCL3). It also prevented toll-like receptor 2 production induced by lipopolysaccharide, interferon, or an anti-CD40 mAb, as well as NF-B function. In THP-1 cells treated with glucocorticoids or IL-10, GILZ was associated with the p65 subunit of NF-B. Activated macrophages in the granulomas of patients with Crohn disease or tuberculosis do not produce GILZ. In contrast, GILZ production persists in tumor-infiltrating macrophages in Burkitt lymphomas. Therefore, GILZ appears to play a key role in the anti-inflammatory and immunosuppressive effects of glucocorticoids and IL-10. Glucocorticoid treatment stimulates GILZ production, reproducing an effect of IL-10, a natural anti-inflammatory agent. The development of delayed-type hypersensitivity reactions is associated with the down-regulation of GILZ gene expression within lesions. In contrast, the persistence of GILZ gene expression in macrophages infiltrating Burkitt lymphomas may contribute to the failure of the immune system to reject the tumor. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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