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  Vol. 32 No. 10, October 1975 TABLE OF CONTENTS
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Myasthenia Gravis and Acetylcholine Receptor

Effect of Steroids in Clinical Course and Cellular Immune Response to Acetylcholine Receptor

Oded Abramsky, MD; Aharon Aharonov, MSc; Dvora Teitelbaum, PhD; Sara Fuchs, PhD

Arch Neurol. 1975;32(10):684-687.


Abstract

• Lymphocytes from patients with myasthenia gravis (MG) were transformed when cultured in vitro with an acetylcholine receptor fraction extracted from the electric organ of an electric eel. Marked diminution of the cellular response to acetylcholine receptor was shown in patients who improved clinically with prednisone treatment. The transient clinical deterioration during the first days of prednisone treatment was accompanied by a transient increase in lymphocyte response. These findings suggest that an in vivo sensitization of lymphocytes to self-acetylcholine receptor may occur in MG, and that a cell-mediated autoimmune mechanism may be important in the pathogenesis of the neuromuscular block. The present observations indicate that prednisone provides a measure of immunosuppression in MG. The transient clinical deterioration during the first days of prednisone therapy may reflect an enhancement of cell reactivity by this drug.



Author Affiliations

From the Department of Chemical Immunology, the Weizmann Institute of Science, Rehovot, Israel (Drs. Abramsky, Teitelbaum, Fuchs and Mr. Aharonov); and the Department of Neurology, Hadassah University Hospital and Hebrew University, Hadassah Medical School, Jerusalem, Israel (Dr. Abramsky).


Footnotes

Accepted for publication Oct 15, 1974.

Reprint requests to the Department of Chemical Immunology, the Weizmann Institute of Science, Rehovot, Israel (Dr. Abramsky).



THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Myasthenia Gravis
Drachman
NEJM 1994;330:1797-1810.
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Acute and Chronic Demyelinating Inflammatory Polyradiculoneuropathy: Association With Autoimmune Diseases and Lymphocyte Response to Human Neuritogenic Protein
Korn-Lubetzki and Abramsky
Arch Neurol 1986;43:604-608.
ABSTRACT  





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