Coculture with autologous myotubes of cytotoxic T cells isolated from muscle in inflammatory myopathies

Ann Neurol. 1991 May;29(5):498-507. doi: 10.1002/ana.410290509.


T-cell lines were expanded from muscle of 10 patients with polymyositis, 5 with inclusion body myositis, 5 with dermatomyositis, and 5 with other muscle diseases. All cell lines uniformly expressed T-cell antigens, but not natural killer cell or B-cell antigens. The proportion of helper (CD4+) and cytotoxic (CD8+) T cells in the expanded lines was variable and showed no correlation with the diagnosis. Sixteen cell lines (6 polymyositis, 4 inclusion body myositis, 5 dermatomyositis, 1 other muscle disease) consisted predominantly of CD8+ T cells. None of these lines displayed natural killer-like cytotoxicity but all were capable of lectin-dependent cytotoxicity. Three of 6 polymyositis, 1 of 4 inclusion body myositis, and 1 of 5 dermatomyositis lines showed low but statistically significant cytotoxicity against autologous myotubes (6 to 27% specific 51Cr release; effector-target ratio, 20:1). The results demonstrate that functionally competent cytotoxic T cells can be expanded from muscle affected by inflammatory myopathies and are consistent with the hypothesis that some cytotoxic T cells recognize an autoantigen on myotubes. Further studies of this experimental system may define the molecular mechanism of T cell-mediated muscle fiber injury and may help to identify the relevant antigens.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antigens, Surface / analysis
  • Cell Adhesion / immunology
  • Clone Cells
  • Cytotoxicity Tests, Immunologic
  • Flow Cytometry
  • HLA Antigens / analysis
  • Humans
  • Interleukin-2 / immunology
  • Killer Cells, Natural / immunology
  • Microscopy, Fluorescence
  • Muscles / immunology*
  • Myositis / immunology*
  • Pilot Projects
  • T-Lymphocytes, Cytotoxic / immunology*
  • T-Lymphocytes, Helper-Inducer / immunology


  • Antigens, Surface
  • HLA Antigens
  • Interleukin-2