Treatment of ongoing experimental myasthenia gravis with short term high dose cyclophosphamide

A. Pestronk, Daniel B Drachman, R. N. Adams

Research output: Contribution to journalArticle

Abstract

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 dose 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 respose 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.

Original languageEnglish (US)
Pages (from-to)79-84
Number of pages6
JournalMuscle and Nerve
Volume5
Issue number1
StatePublished - 1982

Fingerprint

Autoimmune Experimental Myasthenia Gravis
Cholinergic Receptors
Cyclophosphamide
Autoimmune Diseases
Immunologic Memory
Antigens
Torpedo
Antibody-Producing Cells
Neuromuscular Junction
Myasthenia Gravis
Autoantigens
Immunosuppressive Agents
Bone Marrow Transplantation
Pharmaceutical Preparations
B-Lymphocytes
Therapeutics
Antibodies

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Treatment of ongoing experimental myasthenia gravis with short term high dose cyclophosphamide. / Pestronk, A.; Drachman, Daniel B; Adams, R. N.

In: Muscle and Nerve, Vol. 5, No. 1, 1982, p. 79-84.

Research output: Contribution to journalArticle

@article{75efebf4d1bd4192aa7f53902418265d,
title = "Treatment of ongoing experimental myasthenia gravis with short term high dose cyclophosphamide",
abstract = "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 dose 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 respose 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.",
author = "A. Pestronk and Drachman, {Daniel B} and Adams, {R. N.}",
year = "1982",
language = "English (US)",
volume = "5",
pages = "79--84",
journal = "Muscle and Nerve",
issn = "0148-639X",
publisher = "John Wiley and Sons Inc.",
number = "1",

}

TY - JOUR

T1 - Treatment of ongoing experimental myasthenia gravis with short term high dose cyclophosphamide

AU - Pestronk, A.

AU - Drachman, Daniel B

AU - Adams, R. N.

PY - 1982

Y1 - 1982

N2 - 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 dose 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 respose 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.

AB - 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 dose 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 respose 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.

UR - http://www.scopus.com/inward/record.url?scp=0020070976&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020070976&partnerID=8YFLogxK

M3 - Article

C2 - 6977088

AN - SCOPUS:0020070976

VL - 5

SP - 79

EP - 84

JO - Muscle and Nerve

JF - Muscle and Nerve

SN - 0148-639X

IS - 1

ER -