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Treatment of myasthenia gravis with anti-CD4 antibody

Improvement correlates to decreased T-cell autoreactivity

Section of Haematology and Medical Immunology (Drs. Åhlberg, Yi, Holm, and Lefvert), Department of Internal Medicine, Karolinska Hospital; the Department of Neurology (Drs. Pirskanen and Matell), South Hospital; the Department of Clinical Neurophysiology (Dr. Swerup), South Hospital, Stockholm, Sweden; and the Institute of Immunology (Drs. Rieber and Riethmiiller), University of Munich, Munich, Germany.

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.

Address correspondence and reprint requests to Dr. Ann Kari Lefvert, Department of Internal Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden.

Supported by grants from the Swedish Medical Research Council (05646), the Palle Ferb foundation, the Nanna Svartz foundation, and the Karolinska Institute foundations.

Received July 6, 1993. Accepted in final form March 1, 1994.

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