Use of monoclonal antiacetylcholine receptor antibodies to investigate the macrophage inflammation of acute experimental myasthenia gravis: Refractoriness to a second episode of acute disease

A. L. Corey, David P Richman, C. A. Shuman, C. M. Gomez, B. G. Arnason

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The acute phase of experimental autoimmune myasthenia gravis (EAMG) is characterized by macrophage inflammation of muscle endplates and by muscle fiber necrosis. We induced acute EAMG by passive transfer of monoclonal antibodies (mAbs) directed against the acetylcholine receptor (AChR) to investigate this brief and self-limited disorder. After the initial acute phase, animals were refractory to induction of a second episode by subsequent injection of the same mAb, or another anti-AChR mAb of different idiotype and which binds to a separate epitope. Therefore, the refractory state was not caused by an anti-idiotypic response or epitopic modulation. Adoptive transfer of spleen cells from refractory animals had no effect, excluding a role of suppressor lymphocytes, and there was no evidence from experiments involving adoptive transfer of spleen cells from naive animals to refractory animals that refractory animals lacked effector cells.

Original languageEnglish (US)
Pages (from-to)1455-1460
Number of pages6
JournalNeurology
Volume35
Issue number10
StatePublished - 1985
Externally publishedYes

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Autoimmune Experimental Myasthenia Gravis
Acute Disease
Macrophages
Inflammation
Antibodies
Adoptive Transfer
Cholinergic Receptors
Spleen
Muscles
Epitopes
Necrosis
Monoclonal Antibodies
Lymphocytes
Injections

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Use of monoclonal antiacetylcholine receptor antibodies to investigate the macrophage inflammation of acute experimental myasthenia gravis : Refractoriness to a second episode of acute disease. / Corey, A. L.; Richman, David P; Shuman, C. A.; Gomez, C. M.; Arnason, B. G.

In: Neurology, Vol. 35, No. 10, 1985, p. 1455-1460.

Research output: Contribution to journalArticle

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