To study the therapeutic efficacy of IFN-α after the onset of clinical signs of experimental autoimmune myasthenia gravis (EAMG), we treated mice with clinical EAMG with recombinant human IFN-α or mouse IFN-α. In the first experiment, 7 of 16 (44%) mice had a complete clinical remission in the recombinant human IFN-α-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-α group (4/16). In the second experiment, 6 of 18 (33%) mice in the mouse IFN-α-treated group had a complete clinical remission, while none of 17 (0%) mice in the placebo-treated group had remission (p = 0.011). Again, more mice died or worsened in the placebo group (11/17) compared with the IFN-α group (7/18). IFN-α treatment significantly reduced the anti-acetylcholine receptor (AChR) Ab levels, especially the IgG1 and IgG2b isotypes, and the amount of anti-AChR Abs bound to muscle AChR. IFN-α treatment also lowered CD4 cells in the lymph nodes and spleen, and suppressed the in vitro lymphocyte proliferative response to AChR and its dominant peptide in a dose-dependent manner.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Immunology|
|Publication status||Published - Dec 15 1996|
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