TY - JOUR
T1 - IFN-α Therapy Is Effective in Suppressing the Clinical Experimental Myasthenia Gravis
AU - Deng, Caishu
AU - Goluszko, Elzbieta
AU - Baron, Samuel
AU - Wu, Bo
AU - Christadoss, Premkumar
PY - 1996/12/15
Y1 - 1996/12/15
N2 - 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.
AB - 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.
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M3 - Article
C2 - 8955221
AN - SCOPUS:0030589245
SN - 0022-1767
VL - 157
SP - 5675
EP - 5682
JO - Journal of Immunology
JF - Journal of Immunology
IS - 12
ER -