Immune regulatory abnormalities produced by procainamide.

The pathogenesis of procainamide-induced autoantibody production is unknown. To test the effect of procainamide on the immune system, we studied in vitro suppressor cell function and immunoglobulin G (IgG) secretion in 11 patients who developed autoantibodies while taking procainamide. The procainamide group was compared with patients with spontaneous systemic lupus erythematosus (n = 15) and a normal control population (n = 40). Impaired in vitro suppressor cell function was found in 11 of 14 patients with spontaneous systemic lupus erythematosus but in none of the patients taking procainamide. However, total in vitro IgG secretion was significantly increased in the procainamide group with regard to the control and systemic lupus erythematosus groups. There was a direct correlation between the circulating anti-SS DNA antibody titer and in vitro IgG secretion. Furthermore, T cells isolated from the procainamide-treated patients stimulated IgG secretion by normal allogeneic peripheral blood lymphocytes. The added T cells did not affect in vitro suppressor cell function. We postulate that autoantibody production in patients taking procainamide is due to enhanced helper T cell function and not to impaired suppression. However, the development of clinical disease requires the participation of additional genetic or immunologic factors.