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J. Biol. Chem., Vol. 276, Issue 9, 6133-6139, March 2, 2001

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A Specific Interferon (IFN)-stimulated Response Element of the Distal HLA-G Promoter Binds IFN-regulatory Factor 1 and Mediates Enhancement of This Nonclassical Class I Gene by IFN-^*

Sophie Lefebvre^§, Sonia Berrih-Aknin^¶, Francisco Adrian, Philippe Moreau, Sandrine Poea^¶, Luc Gourand, Jean Dausset^**, Edgardo D. Carosella, and Pascale Paul

From the  Service de Recherches en Hémato-Immunologie, Comissariat à l' Energie Atomique, DSV/DRM, Institut d'Hématologie, Hôpital Saint-Louis, Centre Hayem 1, avenue Claude Vellefaux, 75475 Paris cedex 10, France, ^¶ Laboratoire d'Immunologie Cellulaire et Moléculaire, CNRS ESA 8078, Hôpital Marie-Lannelongue, 133, avenue de la Résistance, 92350 Le Plessis Robinson, France,  Hôpital des Bluets, 9 rue des Bluets, 75011 Paris, France, and ^** Fondation Jean Dausset, Centre d'Etude de Polymorphisme Humain, 27, rue Juliette Dodu, 75010 Paris, France

Type I interferons display a broad range of immunomodulatory functions. Interferon  increases gene expression at the transcriptional level through binding of factors to the interferon-stimulated response element (ISRE) within the promoters of interferon-inducible genes, such as HLA class I. Despite mutation of the class I ISRE sequence within the nonclassical HLA-G class I gene promoter, we show that interferon  enhances both transcription and cell surface expression of HLA-G in trophoblasts and amniotic and thymic epithelial cells that selectively express it in vivo. Deletion and mutagenesis analysis of a putative interferon-regulatory factor (IRF)-1 binding site within the HLA-G promoter show that HLA-G transactivation is mediated through an ISRE sequence 746 base pairs upstream from ATG, which is distinct from the interferon-responsive element described within proximal classical class I gene promoters. Electrophoretic mobility shift analysis and supershift analysis further demonstrate that interferon-responsive transcription factors, including IRF-1, specifically bind to the HLA-G ISRE. Our results provide evidence that IRF-1 binding to a functional ISRE within the HLA-G promoter mediates interferon -induced expression of the HLA-G gene. These observations are of general interest considering the implication of HLA-G in mechanisms of immune escape involved in fetal-maternal tolerance and other immune privilege situations.

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