N-acetylprocainamide is a less potent inducer of T cell autoreactivity than procainamide.
We have reported that an inhibitor of DNA methylation, 5-azacytidine, makes cloned, antigen-specific CD4+ T cells autoreactive, and that procainamide and hydralazine mimic this effect. Those results suggested that procainamide and hydralazine may induce autoimmunity by inhibiting DNA methylation and causing T cell autoreactivity. We report now that N-acetylprocainamide, a procainamide derivative that does not induce lupus, is also a DNA methylation inhibitor, but it is 100 times less potent than procainamide in inducing T cell autoreactivity.
Richardson
B
B
University of Michigan Medical Center, Department of Internal Medicine/Rheumatology, Ann Arbor 48109.
Cornacchia
E
E
Golbus
J
J
Maybaum
J
J
Strahler
J
J
Hanash
S
S
D000120:Acecainide / Q000494:pharmacology*; D001323:Autoantibodies; D001327:Autoimmune Diseases / Q000139:chemically induced; D002851:Chromatography, High Pressure Liquid; D004247:DNA / Q000037:antagonists & inhibitors*; D006801:Humans; D006830:Hydralazine / Q000494:pharmacology; D066298:In Vitro Techniques; D008745:Methylation; D010793:Phthalazines / Q000494:pharmacology; D011342:Procainamide / Q000031:analogs & derivatives* / Q000494:pharmacology; D013601:T-Lymphocytes / Q000187:drug effects*
D001323:Autoantibodies; D010793:Phthalazines; D006830:Hydralazine; D004247:DNA; D000120:Acecainide; C043388:phthalazine; D011342:Procainamide