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Treatment of ongoing experimental myasthenia gravis with short term high dose cyclophosphamide
Author(s) -
Pestronk Alan,
Drachman Daniel B.,
Adams Robert N.
Publication year - 1982
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880050115
Subject(s) - myasthenia gravis , cyclophosphamide , acetylcholine receptor , medicine , immunology , neuromuscular junction , antibody , autoimmune disease , antigen , receptor , chemotherapy , biology , neuroscience
We have treated animals with an ongoing autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), using a strategy designed to eliminate the antibody‐producing cells. During well‐established EAMG, a single high doese of cyclophosphamide was given because of its known effectiveness against B‐lymphocytes. To counteract the lethal effects of the drug, the rats were “rescued” by bone marrow cell transplantation. This treatment produced a rapid and sustained fall of antibody titers against both the immunizing antigen ( Torpedo acetylcholine receptor) and the autoantigen (rat acetylcholine receptor). Immunologic memory, as measured by an anamnestic response to the antigen, was partially suppressed. Cyclophosphamide treatment produced improvement in the neuromuscular defect: treated animals had, on the average, twice as many acetylcholine receptors at neuromuscular junctions compared with untreated EAMG animals. This treatment method of short‐term high doses of an immunosuppressive drug, such as cyclophosphamide, may eventually prove useful for human myasthenia gravis and other autoimmune diseases.