R. Ahlberg et al., TREATMENT OF MYASTHENIA-GRAVIS WITH ANTI-CD4 ANTIBODY - IMPROVEMENT CORRELATES TO DECREASED T-CELL AUTOREACTIVITY, Neurology, 44(9), 1994, pp. 1732-1737
We treated a patient with severe myasthenia gravis with a chimeric (mu
rine/human) anti-CD4 monoclonal antibody (cM-T412) for 7 days and foll
owed the therapeutic effect by standardized muscle function tests, sin
gle-fiber electromyography, and immunologic examinations of disease-sp
ecific B- and T-cell functions. Clinical and electrophysiologic improv
ement began within 4 days, lasted for 3 months, and was maximal betwee
n days 16 and 58. The CD4+ lymphocytes decreased to a minimum of 80 ce
lls per mu 1 of peripheral blood, recovered slowly during the first ye
ar of follow-up, and did not correlate with changes in disease severit
y. T-cell stimulation by human acetylcholine receptor was abolished by
the treatment but became detectable at the time of worsening of sympt
oms. The concentration of acetylcholine receptor antibodies in serum w
as not decreased by the treatment. The results suggest that anti-CD4 a
ntibody administration could be effective in the treatment of severe m
yasthenia gravis and indicate that acetylcholine receptor-specific T l
ymphocytes might contribute to the disturbed neuromuscular transmissio
n in the disease.