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Blood, 1 March 2006, Vol. 107, No. 5, pp. 2037-2044.
Prepublished online as a Blood First Edition Paper on November 17, 2005; DOI 10.1182/blood-2005-07-2760.
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IMMUNOBIOLOGY
GILZ expression in human dendritic cells redirects their maturation and prevents antigen-specific T lymphocyte response
Nicolas Cohen,
Enguerran Mouly,
Haifa Hamdi,
Marie-Christine Maillot,
Marc Pallardy,
Véronique Godot,
Francis Capel,
Axel Balian,
Sylvie Naveau,
Pierre Galanaud,
François M. Lemoine, and
Dominique Emilie
From the INSERM UMR-S764, Service d'Hépato-Gastro-Entérologie and Service de Microbiologie—Immunologie Biologique, Hôpital Antoine Béclère, Assistance Publique-Hôpitaux de Paris, Institut Paris-Sud sur les Cytokines, Université Paris-Sud, Clamart, France; CNRS UMR 7087/UPMC, Hôpital Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, France; and INSERM UMR-S749, Faculté de Pharmacie, Université Paris-Sud, Châtenay-Malabry, France.
Interleukin (IL)-10 and glucocorticoids (GCs) inhibit the ability of antigen-presenting dendritic cells (DCs) to stimulate T lymphocytes. We show that induction of GILZ (GC-induced leucine zipper) is involved in this phenomenon. IL-10, dexamethasone (DEX), and transforming growth factor (TGF) stimulate GILZ production in human immature DCs derived from monocytes and from CD34+ cells. GILZ is necessary and sufficient for DEX, IL-10, and TGF modulation of CD80, CD83, CD86, immunoglobulin-like transcript (ILT)-3, and B7-H1 expression by DCs, and alteration of DC functions. GILZ stimulates the production of IL-10 by immature DCs and prevents the production of inflammatory chemokines by CD40L-activated DCs. In contrast, GILZ does not prevent CD40 ligand-mediated inhibition of phagocytosis, indicating that it affects some but not all aspects of DC maturation. GILZ prevents DCs from activating antigen-specific T lymphocyte responses. Administration of GCs to patients stimulates GILZ expression in their circulating antigen-presenting cells, and this contributes to the weak lymphocyte responses of GC-treated patients. Thus, regulation of GILZ expression is an important factor determining the decision of DCs whether or not to stimulate T lymphocytes, and IL-10, GCs, and TGF share this mechanism for influencing DC functions and the balance between immune response and tolerance.
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