TY - JOUR
T1 - Treatment of myasthenia gravis with anti–CD4 antibody
T2 - Improvement correlates to decreased T–cell autoreactivity
AU - Åhlberg, R.
AU - Yi, Q.
AU - Pirskanen, R.
AU - Matell, G.
AU - Swerup, C.
AU - Rieber, E. P.
AU - Riethmüller, G.
AU - Holm, G.
AU - Lefvert, Ann Kari
PY - 1994/9
Y1 - 1994/9
N2 - We treated a patient with severe myasthenia gravis with a chimeric (murine/human) anti–CD4 monoclonal antibody (cM–T412) for 7 days and followed the therapeutic effect by standardized muscle function tests, single–fiber electromyography, and immunologic examinations of disease–specific B– and T–cell functions. Clinical and electrophysiologic improvement began within 4 days, lasted for 3 months, and was maximal between days 16 and 58. The CD4= lymphocytes decreased to a minimum of 80 cells per μl of peripheral blood, recovered slowly during the first year of follow–up, and did not correlate with changes in disease severity. T–cell stimulation by human acetylcholine receptor was abolished by the treatment but became detectable at the time of worsening of symptoms. The concentration of acetylcholine receptor antibodies in serum was not decreased by the treatment. The results suggest that anti–CD4 antibody administration could be effective in the treatment of severe myasthenia gravis and indicate that acetylcholine receptor–specific T lymphocytes might contribute to the disturbed neuromuscular transmission in the disease.
AB - We treated a patient with severe myasthenia gravis with a chimeric (murine/human) anti–CD4 monoclonal antibody (cM–T412) for 7 days and followed the therapeutic effect by standardized muscle function tests, single–fiber electromyography, and immunologic examinations of disease–specific B– and T–cell functions. Clinical and electrophysiologic improvement began within 4 days, lasted for 3 months, and was maximal between days 16 and 58. The CD4= lymphocytes decreased to a minimum of 80 cells per μl of peripheral blood, recovered slowly during the first year of follow–up, and did not correlate with changes in disease severity. T–cell stimulation by human acetylcholine receptor was abolished by the treatment but became detectable at the time of worsening of symptoms. The concentration of acetylcholine receptor antibodies in serum was not decreased by the treatment. The results suggest that anti–CD4 antibody administration could be effective in the treatment of severe myasthenia gravis and indicate that acetylcholine receptor–specific T lymphocytes might contribute to the disturbed neuromuscular transmission in the disease.
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U2 - 10.1212/wnl.44.9.1732
DO - 10.1212/wnl.44.9.1732
M3 - Article
C2 - 7936306
AN - SCOPUS:0028101460
SN - 0028-3878
VL - 44
SP - 1732
EP - 1737
JO - Neurology
JF - Neurology
IS - 9
ER -