5-Azacytidine induced inhibition of mitogenic response by agents that activate or augment activation of human peripheral blood T lymphocytes.
Previous work from our laboratory demonstrated the mitogenic response of human peripheral blood T lymphocytes by phytohemagglutinin (PHA), phorbol myristate acetate (PMA) and ionomycin, or interleukin 2 (IL-2). Increasing levels of incorporated 5-azacytosine inhibited the action of the methyltransferase suggesting that incorporation of 5-azacytosine into DNA could be responsible for the inhibiting effect of 5-azacytidine (5-aza-CR) on DNA methylation. In this study, we first demonstrated the inhibition of mitogenic response by agents, such as PHA, PMA and ionomycin, or IL-2, that activate or augment activation of human peripheral blood T cells by treatment of the analog 5-azacytidine. Over 1 microM of 5-azacytidine, we detected significant inhibition of proliferative response and over 5 microM of 5-azacytidine toxic effect of cell viability. We found no significant change of T cell subsets after treatment of 5-azacytidine.
D000328:Adult; D001374:Azacitidine / Q000494:pharmacology*; D004987:Ethers / Q000494:pharmacology; D005260:Female; D006801:Humans; D015759:Ionomycin; D008213:Lymphocyte Activation; D008297:Male; D010835:Phytohemagglutinins / Q000494:pharmacology; D012397:Rosette Formation; D013601:T-Lymphocytes / Q000187:drug effects*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013936:Thymidine / Q000378:metabolism
D004987:Ethers; D010835:Phytohemagglutinins; D015759:Ionomycin; D001374:Azacitidine; D013755:Tetradecanoylphorbol Acetate; D013936:Thymidine