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    Differential patterns of methylation of the IFN promoter at CpG and non-CpG sites underlie differences in IFN gene expression between human neonatal and adult CD45RO- T-cells

    Access Status
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    Authors
    White, Greg
    Watt, P.
    Holt, B.
    Holt, P.
    Date
    2002
    Type
    Journal Article
    
    Metadata
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    Citation
    White, Gregory P. and Watt, Paul M. and Holt, Barbara J. and Holt, Patrick G.. 2002. Differential patterns of methylation of the IFN promoter at CpG and non-CpG sites underlie differences in IFN gene expression between human neonatal and adult CD45RO- T-cells. Journal of Immunology 168 (6): 2820-2827.
    Source Title
    Journal of Immunology
    Additional URLs
    http://www.jimmunol.org/cgi/content/abstract/168/6/2820
    Faculty
    Curtin Business School
    School of Accounting
    URI
    http://hdl.handle.net/20.500.11937/24398
    Collection
    • Curtin Research Publications
    Abstract

    IFN- is a potent pleiotropic Th1 cytokine, the production of which is tightly regulated during fetal development. Negative control of fetal/neonatal IFN- production is generally attributed to the Th1-antagonistic effect of mediators produced by the placenta, but evidence exists of additional and more direct transcriptional regulation. We report that neonatal (cord blood) CD3+/CD45RO- T cells, in particular the CD4+/CD45RO- subset, are hypermethylated at CpG and non-CpG (CpA and CpT) sites within and adjacent to the IFN- promoter. In contrast, CpG methylation patterns in cord blood IFN--producing CD8+/CD45RO- T cells and CD56+/CD16+/CD3- NK cells did not differ significantly from those in their adult counterparts. Consistent with this finding, IFN- production by stimulated naive cord blood CD4+ T cells is reduced 5- to 10-fold relative to adult CD4+ T cells, whereas production levels in neonatal and adult CD8+ T cells are of a similar order. Evidence of significant CpA and CpT methylation was not discovered in promoter sequence from other cytokines (IL-4, TNF-, or IFN-R -chain). We additionally demonstrate that overexpression of DNA methyltransferase 3a in embryonic kidney carcinoma cells is accompanied by CpA methylation of the IFN- promoter

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