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Volume 271, Number 43, Issue of October 25, 1996 pp. 26783-26793
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Retinoic Acid-induced Transcriptional Modulation of the Human Interferon- Promoter

(Received for publication, July 29, 1996)

Marco Cippitelli , Jianping Ye ^§ , Vincenzo Viggiano ^§ , Antonio Sica ^§ , Paritosh Ghosh ^§ , Alberto Gulino ^¶ , Angela Santoni ^'' and Howard A. Young ^§

From the  Intramural Research Support Program, Scientific Application International Corporation Frederick, and the ^§ Laboratory of Experimental Immunology, Division of Basic Science, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201, the ^¶ Department of Experimental Medicine, University of L'Aquila, 67100 L'Aquila, Italy, the  Department of Experimental Medicine and Pathology, University ``La Sapienza,'' Roma 00158, Italy, and the ^'' Laboratory of Pathophysiology, Regina Elena Cancer Institute, Roma 00158, Italy

Disregulation of vitamin A metabolism is able to generate different immunological effects, including altered response to infection, reduced IgG production, and differential regulation of cytokine gene expression (including interleukin-2 and -4 and interferon- (IFN-)). In particular, IFN- gene expression is significantly affected by vitamin A and/or its derivatives (e.g. retinoic acid (RA)). Here, we analyze the effect of retinoic acid on IFN- transcription. Transient transfection assays in the human T lymphoblastoid cell line Jurkat demonstrated that the activation of the IFN- promoter was significantly down-regulated in the presence of RA. Surprisingly, two different AP-1/CREB-ATF-binding elements situated in the initial 108 base pairs of the IFN- promoter and previously shown to be critical for transcriptional activity were unaffected by RA. Utilizing promoter deletions and electrophoretic mobility shift analysis, we identified a USF/EGR-1-binding element cooperating in the modulation of IFN- promoter activity by RA. This element was found to be situated in a position of the IFN- promoter close to a silencer element previously identified in our laboratory. These results suggest that direct modulation of IFN- promoter activity is one of the possible mechanisms involved in the inhibitory effect of retinoids on IFN- gene expression.

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