Anti-idiotypic T cells in early stages of myasthenia gravis: increase in the number and prevalence correlated to clinical improvement in patients. Academic Article uri icon

Overview

abstract

  • An idiotypic network involving T and B cells bearing complementary structures has been suggested to be important for the regulation of immune response in healthy and disease situations. A previous study by the authors has demonstrated the presence of a relatively higher concentration of anti-idiotypic antibodies than of idiotypic in early myasthenia gravis (MG), suggesting that the development of an anti-idiotypic immunity is important in early MG. The present study was conducted to examine the cellular components of the idiotypic network in the same situation. T and B cells reactive to acetylcholine receptor (AChR) or to a disease-related idiotype and to an anti-idiotype were analysed in seven patients with early MG at various times after the start of the disease. The results show that a significant increase in the number of idiotype-reactive interferon-gamma-secreting T cells and a shift from AChR-reactive to idiotype- and/or anti-idiotype-reactive T cells in the patients at 6 month follow-up were noted. Such changes seem to correlate to a clinical improvement in the patients. The enhanced anti-idiotypic T-cell response and the clinical improvement in the patients may speak in favour of a role for the anti-idiotypic immunity in controlling the autoimmune response in MG, i.e., down-regulating autoantibody-producing B cells and idiotypic (AChR-specific) T cells. Thus, an immune intervention towards the enhancement of the anti-idiotypic immunity in patients might be a rewarding approach. Further studies with regard to cell interactions and immune regulations in the network are warranted.

publication date

  • December 1, 1996

Research

keywords

  • Antibodies, Anti-Idiotypic
  • Autoantibodies
  • Autoantigens
  • Myasthenia Gravis
  • Receptors, Cholinergic
  • T-Lymphocytes

Identity

Scopus Document Identifier

  • 0029823115

Digital Object Identifier (DOI)

  • 10.1046/j.1365-3083.1996.d01-356.x

PubMed ID

  • 8972746

Additional Document Info

volume

  • 44

issue

  • 6