Abstract

The authors suggest that the same population of antibodies responsible for AChR precipitation in radioimmunoassay is also responsible for enhanced endocytosis in rat myotube cultures. However, AChR antibodies may be only one of several possible factors responsible for myasthenic junctional defect. Antibody titers are not a precise index of clinical symptomatology, especially following thymectomy, where in most cases titers do not parallel the clinical state. Furthermore, in neonatal MG, 80% of myasthenic mothers have AChR antibodies, whereas only 12% of their offspring have neonatal myasthenia. We recently studied a case in which AChR antibodies were associated with myasthenia in the infant and yet were derived from a mother who was in remission from MG. This case, together with the thymectomy results, suggests that in addition to AChR antibodies, other factors - such as hormones, cellular as well as humoral immune factors, or the state of the neuromuscular junction - may be necessary to produce functional defects at the neuromuscular junction.

Original languageEnglish (US)
Number of pages1
JournalMuscle and Nerve
Volume1
Issue number4
StatePublished - Jan 1 1978

ASJC Scopus subject areas

  • Physiology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Physiology (medical)

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