IFN-ALPHA THERAPY IS EFFECTIVE IN SUPPRESSING THE CLINICAL EXPERIMENTAL MYASTHENIA-GRAVIS

To study the therapeutic efficacy of IFN-alpha after the onset of clin ical signs of experimental autoimmune myasthenia gravis (EAMC), we tre ated mice with clinical EAMC with recombinant human IFN-alpha or mouse IFN-alpha. In the first experiment, 7 of 16 (44%) mice had a complete clinical remission in the recombinant human IFN-alpha-treated group, in contrast to none in the placebo group (0/14) (p = 0.006). There was a higher incidence of death and severe disease in the placebo group ( 7/14) relative to the IFN-alpha group (4/16). In the second experiment , 6 of 18 (33%) mice in the mouse IFN-alpha-treated group had a comple te clinical remission, while none of 17 (0%) mice in the placebo-treat ed group had remission (p = 0.011), Again, more mice died or worsened in the placebo group (11/17) compared with the IFN-alpha group (7/18), IFN-alpha treatment significantly reduced the anti-acetylcholine rece ptor (AChR) Ab levels, especially the IgG1 and IgG2b isotypes, and the amount of anti-AChR Abs bound to muscle AChR. IFN-alpha treatment als o lowered CD4 cells in the lymph nodes and spleen, and suppressed the in vitro lymphocyte proliferative response to AChR and its dominant pe ptide in a dose-dependent manner.