IFN-alpha therapy is effective in suppressing the clinical experimental myasthenia gravis.

Abstract

To study the therapeutic efficacy of IFN-alpha after the onset of clinical signs of experimental autoimmune myasthenia gravis (EAMG), we treated mice with clinical EAMG 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 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-alpha group (7/18). IFN-alpha 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-alpha 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.

• Authors: C Deng, E Goluszko, S Baron, B Wu, P Christadoss
• Journal: Journal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 157 Issue 12 Pg. 5675-82 (Dec 15 1996) ISSN: 0022-1767 [Print] United States
• PMID: 8955221 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Autoantibodies
• CD4 Antigens
• CD8 Antigens
• Immunodominant Epitopes
• Immunoglobulin Isotypes
• Interferon Type I
• Receptors, Nicotinic
• Recombinant Proteins

Topics

• Animals
• Autoantibodies (immunology, metabolism)
• CD4 Antigens (metabolism)
• CD8 Antigens (metabolism)
• Humans
• Immunodominant Epitopes
• Immunoglobulin Isotypes (immunology)
• Interferon Type I (therapeutic use)
• Lymphocyte Activation
• Male
• Mice
• Mice, Inbred C57BL
• Muscles (immunology)
• Myasthenia Gravis (drug therapy)
• Receptors, Nicotinic (immunology)
• Recombinant Proteins