Thymic B cells from myasthenia gravis patients are activated B cells. Phenotypic and functional analysis

J Immunol. 1990 Oct 1;145(7):2115-22.

Abstract

Thymic cell populations from 12 patients displaying myasthenia gravis were submitted to a phenotypic and functional study. Immunofluorescence analysis of thymic sections revealed the presence in germinal centers of B lymphocytes expressing the B cell markers--CD19, CD21, IgD, or IgM. After T cell and macrophage depletion of thymic single cell suspensions, B cell-enriched populations were isolated. Enriched B cells expressed at variable levels activation markers such as CD71, 4F2, CD23, and B8.7, indicating that a marked proportion of them are activated. Moreover, addition of B cell growth factor 12kDa and to a lesser extent of rIL-2 induced a spontaneous proliferation of these B cell populations. These functional and phenotypic signs of activation may reveal the first steps of an autoimmune response against acetylcholine receptor as enriched B cell populations have the capacity to spontaneously secrete anti-acetylcholine receptor antibody.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antibody Formation
  • Antigens, CD / analysis
  • Antigens, Differentiation, B-Lymphocyte / analysis
  • Antigens, Differentiation, T-Lymphocyte / analysis
  • Autoantibodies / biosynthesis
  • B-Lymphocytes / immunology*
  • Female
  • Fluorescent Antibody Technique
  • Humans
  • Interleukin-2 / pharmacology
  • Interleukin-4 / pharmacology
  • Lymphocyte Activation
  • Male
  • Myasthenia Gravis / immunology*
  • Myasthenia Gravis / pathology
  • Receptors, Fc / analysis
  • Receptors, IgE
  • Receptors, Nicotinic / immunology
  • T-Lymphocytes / immunology
  • Thymectomy
  • Thymus Gland / immunology*
  • Thymus Gland / pathology

Substances

  • Antigens, CD
  • Antigens, Differentiation, B-Lymphocyte
  • Antigens, Differentiation, T-Lymphocyte
  • Autoantibodies
  • Interleukin-2
  • Receptors, Fc
  • Receptors, IgE
  • Receptors, Nicotinic
  • Interleukin-4