Fas and Fas ligand interaction induces apoptosis in inflammatory myopathies: CD4+ T cells cause muscle cell injury directly in polymyositis

Arthritis Rheum. 1999 Feb;42(2):291-8. doi: 10.1002/1529-0131(199902)42:2<291::AID-ANR11>3.0.CO;2-1.

Abstract

Objective: To investigate the involvement of the Fas/Fas ligand (Fas/FasL) system in the inflammatory myopathies.

Methods: Frozen muscle sections obtained from 7 patients with polymyositis (PM), 4 patients with dermatomyositis (DM), and 3 controls were studied by immunochemistry. Apoptosis was detected by DNA electrophoresis and in situ labeling using the TUNEL method.

Results: Fas was detected on muscle fibers and infiltrating mononuclear cells (MNC) in 6 PM patients and 2 DM patients. FasL was expressed mainly on CD4+ T cells and some CD8+ T cells, and on macrophages surrounding Fas-positive muscles in 4 PM patients and 1 DM patient. In 3 of the 5 patients with FasL-positive MNC, the TUNEL method showed that both invaded myonuclei and MNC underwent apoptosis. Chromosomal DNA from the muscle tissue of these patients showed ladder formation.

Conclusion: Fas/FasL is involved in muscle cell apoptosis in at least 2 of the inflammatory myopathies, PM and DM. Although CD8+-mediated cytotoxicity is thought to be the main mechanism of muscle injury in PM, our data suggest that CD4+ T cells also directly cause muscle cell damage.

MeSH terms

  • Apoptosis*
  • CD4-CD8 Ratio
  • CD4-Positive T-Lymphocytes / metabolism*
  • CD8-Positive T-Lymphocytes / metabolism
  • DNA / analysis
  • Dermatomyositis / metabolism*
  • Dermatomyositis / pathology
  • Fas Ligand Protein
  • Female
  • Humans
  • In Situ Nick-End Labeling
  • Leukocytes, Mononuclear / metabolism
  • Male
  • Membrane Glycoproteins / metabolism*
  • Middle Aged
  • Muscle Fibers, Skeletal / metabolism
  • Muscle Fibers, Skeletal / pathology
  • Muscle, Skeletal / metabolism*
  • Muscle, Skeletal / pathology
  • Polymyositis / metabolism*
  • Polymyositis / pathology
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • fas Receptor / metabolism*

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • Proto-Oncogene Proteins c-bcl-2
  • fas Receptor
  • DNA