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Promoter Is Hypomethylated from Early T Cell Development through Mature Naive and Th1 Cell Differentiation, but Is Hypermethylated in Th2 Cells
Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
Reports on the status of DNA methylation of the IFN-
gene during T cell development in human and mouse have presented somewhat contradictory results. In this study we demonstrate in the mouse that methylation of the IFN- promoter inhibits its transcriptional activity, and define a small hypomethylated region in T cells that correlates with transcription. The IFN- promoter was also hypomethylated in NK cells, but not in B cells or nonhemopoietic tissues. Surprisingly, unlike the promoters of the IL-2 and IL-4 genes, the IFN- promoter was hypomethylated in naive CD4+ and CD8+ T cells, and in this form from very early in T cell development. A population of non-B, non-T, non-NK cells containing the hypomethylated promoter was also found in the bone marrow. The hypomethylated state appears stable until peripheral CD4+ T cells differentiate in response to Ag and APC. After T cell stimulation in vitro under Th2 conditions, but far less so under Th1 conditions, CD4+ cells display a more methylated IFN- promoter, which may contribute to the lack of expression of IFN- in these preactivated cells. Our experiments support a new model of IFN- chromatin structural changes in murine T cell development that differs from what has been previously published for human T cells.
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