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The Journal of Immunology, 2000, 164: 4143-4149.
Copyright © 2000 by The American Association of Immunologists

Methylation of Class II trans-Activator Promoter IV: A Novel Mechanism of MHC Class II Gene Control1

Ann C. Morris, Wendi E. Spangler and Jeremy M. Boss2

Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322

Inhibition of class II trans-activator (CIITA) expression prevents embryonic trophoblast cells from up-regulating MHC class II genes in response to IFN-{gamma}. This is thought to be one mechanism of maternal tolerance to the fetal allograft. The CIITA gene is regulated by four distinct promoters; promoter III directs constitutive (B cell) expression, and promoter IV regulates IFN-{gamma}-inducible expression. Using in vivo genomic footprinting, promoter-reporter analysis, Southern blot analysis, and RT-PCR, we have examined the cause of CIITA silencing in a trophoblast-derived cell line. We report here that methylation of promoter IV DNA at CpG sites in Jar cells prevents promoter occupancy and IFN-{gamma}-inducible transcription. The inhibition of CpG methylation in Jar cells by treatment with 5-aza-2'-deoxycytidine restores IFN-{gamma} inducibility to CIITA. This is the first description of an epigenetic mechanism involved in regulation of CIITA and MHC class II gene expression.







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