Treatment of mice with established autoimmunity to acetylcholine receptor (AChR) with interferon a (EFNα) suppressed experimental autoimmune myasthenia gravis (EAMG) (Shenoy et al, J. Immunology, 154:6203, 1995). To study the therapeutic efficacy of IFNα after the established clinical signs, we treated mice with established EAMG with mouse IFNα (mIFNα) or human recombinant IFNα (HurlFNα). In experiment I, mIFNα ICPU and in experiment II, HurlFNα 104 U was ?iven intraperitoneal 3 times a week for 6 weeks. In experiment 1,6 of 8 (33%) mice had a complete clinical remission or significant improvement in IFNα group, while only 1 of 17 (6%) mice improved in PBS group, p=0.047; more mice died or worsened in PBS group (11/17) compared to IFNα group (8/18); In experiment II, 7 of 16 (44%) mice had a complete remission or significant improvement in IFNα group, in contrast to only 1 of 14 (7%) in PBS group, p=0.027; also more mice died or worsened in PBS group (6/14) than in IFNα group (4/16). IFNα treatment reduced the MHC class II expression on peripheral blood lymphocytes, and lowered the serum IFNγ level. IFNα in vitro also suppressed AChR and its dominant peptide a!46-162 specific lymphocyte proliferation. Therefore, IFNα, one of the very few treatments which exerts a therapeutic effect on EAMG, is associated with down regulation of IFNγ, MHC class II, and lymphocyte activation. Supported by MDA,Myasthenia Gravis Foundation Osserman postdoctoral fellow.J.W.McLaughlin postdoctoral fellow.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology