Autologous mixed lymphocyte reaction in patients with myasthenia gravis: correlation with disease activity.


Journal Article

Enriched subpopulations of peripheral blood mononuclear cells from patients with myasthenia gravis and from normal control individuals were tested for proliferative ability in the autologous mixed lymphocyte reactions. Myasthenia gravis patients were studied at various phases of therapy. Longitudinal patient populations were studied. Purified T cells from untreated patients with active myasthenia gravis demonstrated enhanced proliferative responses when co-cultured with nonmodified autologous non-T cells. Furthermore, treatment by thymectomy with or without prior plasmapheresis was associated with a consequent normalization of the autologous reaction. The enhanced autologous mixed lymphocyte reaction in the pre-treatment group of myasthenia gravis patients was significantly different from the post-treatment and normal control groups (Stimulation Index, p less than 0.01 and p less than 0.02, respectively). This difference in activity was also confirmed in a longitudinal study of 10 patients followed pre- and post-treatment (Stimulation Index, p less than 0.02). There was no difference between the responses of post-treatment patients and normal control individuals. There was no evidence of altered T cell responsiveness or non-T cell stimulation, as measured by the allogeneic mixed lymphocyte reaction or by mitogen-induced lymphocyte proliferation, between pretreatment and post-treatment patients as compared to controls. The responses were not affected by serum substitution experiments whereby myasthenic responder T cells were co-cultured with pooled normal human sera. Other parameters studied included clinical status, anti-acetylcholine receptor antibody levels, and thymic pathology. An intriguing connection between abnormalities in the thymic cell populations and the autoaggressive state in myasthenia may be reflected by the in vitro autologous mixed lymphocyte reaction.

Full Text

Cited Authors

  • Greenberg, SJ; Olanow, CW; Dawson, DV; Crane, B; Roses, AD

Published Date

  • March 1, 1984

Published In

Volume / Issue

  • 132 / 3

Start / End Page

  • 1229 - 1236

PubMed ID

  • 6229579

Pubmed Central ID

  • 6229579

Electronic International Standard Serial Number (EISSN)

  • 1550-6606

International Standard Serial Number (ISSN)

  • 0022-1767


  • eng