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Prepublished online as a Blood First Edition Paper on September 12, 2002; DOI 10.1182/blood-2002-02-0538.
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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.
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