Preservation of T-lymphocyte activity in autoimmune MRL-lpr mice treated with prostaglandin

MRL-lpr mice display immunoregulatory disturbances which are related to an early massive T-lymphocyte hyperplasia. Features of autoimmunity are rapidly progressive and these animals die from immune complex-mediated glomerulonephritis. Previous studies show that 15 methyl prostaglandin E1 (PGE) treatment in MRL-lpr mice prolongs survival by preventing lymphoproliferation and the subsequent renal disease. The present study indicates that a major activity of this therapy stabilizes several T-cell functions. Both the age-related loss of the autologous mixed-lymphocyte reaction (AMLR) (Ly1+ 2,3- dependent) and the concanavalin A-induced suppressor cell activity (Ly1- 2,3+ dependent) remain intact. It is suggested that PGE preserves these T-cell functions by maintaining a more normal balance of T-cell subsets.