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¹ UPRES EA 219, Service d'Anatomie Pathologique
² Unité Mixte de Recherche 8603 Centre National de la Recherche Scientifique (CNRS)/Université Paris-V, Institut Fédératif de Recherche Necker-Enfants Malades, Hopital Necker-Enfants Malades, 75743 Paris Cedex 15, France
³ Unité Institut National de la Santé et de la Recherche Médicale (INSERM) 429, Institut Fédératif de Recherche Necker-Enfants Malades, Hopital Necker-Enfants Malades, 75743 Paris Cedex 15, France
⁴ Department of Biochemistry and Molecular Biology, University of Parma, 43100 Parma, Italy
⁵ Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC)/CNRS/INSERM/ULP and Collège de France, 67404 Illkirch, France

Address correspondence to Frédéric Geissmann, Service d'Anatomie Pathologique EA 219, Hopital Necker-Enfants Malades, 161 rue de Sevres, 75743 Paris Cedex 15, France. Phone: 33-1-44-49-06-75; Fax: 33-1-44-49-06-76; email: geissman{at}necker.fr

Maturation of dendritic cells (DCs) is a critical step for the induction of an immune response. We have examined the role of retinoid nuclear receptor pathways in this process. Retinoids induce DC apoptosis, in the absence of inflammatory signals, through retinoic acid receptor (RAR)/retinoic X receptor (RXR) heterodimers. In contrast, via a cross talk with inflammatory cytokines, retinoids increase DNA binding activity of nuclear factor B in DCs, trigger membrane major histocompatibility complex class II and costimulatory molecule expression, induce the differentiation of immature DCs into mature DCs, and enhance antigen-specific T cell response. This maturation of DCs is mediated via a RXR-dependent/RAR-independent pathway and via an RAR/RXR pathway distinct from the one responsible for apoptosis. Apoptosis and activation, mediated through distinct nuclear retinoid receptor pathways, can be dissociated from each other with selective synthetic retinoids. We identify a novel cellular function for retinoids and suggest that selective retinoids might be of interest for controlling antigen presentation.

Key Words: human • cellular activation • antigen presentation • immunomodulators • nuclear receptors

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