NDLI: HLA-G gene repression is reversed by demethylation.

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HLA-G gene repression is reversed by demethylation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dausset, Jean Carosella, Edgardo D. Rousseau, Philippe Moreau, Philippe Mouillot, Gael Marcou, Celine
Description	Author Affiliation: Moreau P ( Commissariat à l'Energie Atomique, Service de Recherche en Hémato-Immunologie, Direction des Sciences du Vivant/Department de Recherche Médicale, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, 75010 Paris, France. moreau@dsvidf.cea.fr);
Abstract	The HLA-G molecule plays an important role in immune tolerance, protecting the fetus from maternal immune attack, and probably contributes to graft tolerance and tumor escape from the host immune system. HLA-G expression is tightly regulated and involves mechanisms acting in part at the transcriptional level. Nevertheless, almost all regulatory sequences that govern constitutive and inducible HLA class I gene transcription are disrupted in the HLA-G gene promoter, suggesting an unusual regulatory process. In further investigating the molecular mechanisms of HLA-G gene activation, we evaluated the influence of epigenetic mechanisms on seven HLA-G-negative cell lines that exhibit various phenotypes. Exposure of cells to histone deacetylase inhibitors, or to the demethylating agent 5-aza-2'-deoxycytidine, revealed that HLA-G gene transcription is inhibited by DNA methylation. Reversal of methylation-mediated repression may directly induce HLA-G cell-surface expression, supporting the idea that HLA-G might be activated by such a mechanism during malignancy, inflammation, and allogenic reactions.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	3
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Azacitidine Analogs & Derivatives DNA Methylation HLA Antigens Biosynthesis Genetics Histocompatibility Antigens Class I Pharmacology Blotting, Southern Blotting, Western Dose-Response Relationship, Drug Enzyme Inhibitors Flow Cytometry HLA-G Antigens Histone Deacetylases Immunohistochemistry Reverse Transcriptase Polymerase Chain Reaction Time Factors Transcription, Genetic Tumor Cells, Cultured Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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