Role of T lymphocytes in experimental Staphylococcus aureus arthritis

Scand J Immunol. 1994 Apr;39(4):403-8. doi: 10.1111/j.1365-3083.1994.tb03392.x.


Using a recently developed murine model of haematogenously induced Staphylococcus aureus, the authors have characterized the phenotypes and functional properties of inflammatory cells present in the synovium of arthritic mice. The results show that large numbers of granulocytes and macrophages were observed in the inflamed synovia within 24 h of inoculation of S. aureus strain LS-1. Many of the synovial macrophage-like cells strained for cytoplasmic IL-1 alpha and TNF-alpha. Subsequently (> or = 48 h later), a prominent infiltration of T lymphocytes, predominantly of CD4+ phenotype, was observed. Some of the T lymphocytes stained for IL-2 receptor and intracytoplasmic interferon-gamma (IFN-gamma). Surprisingly, in spite of the severe inflammatory process, very few cells expressed MHC class-II molecules in the arthritic synovia. In addition, in vivo depletion of CD4+ T-cells resulted in a considerably milder course of staphylococcal arthritis. The similarities in the phenotype expression of synovial cells and central role of T-cells in S. aureus arthritis as well as in non-infectious models of arthritis, indicate that the process governing joint destruction is likely to be the same, irrespective of the initial stimulus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arthritis, Infectious / etiology*
  • Arthritis, Infectious / immunology
  • Arthritis, Infectious / pathology
  • Disease Models, Animal
  • Immunohistochemistry
  • Interferon-gamma / metabolism
  • Interleukin-1 / metabolism
  • Lymphocyte Depletion
  • Male
  • Mice
  • Phenotype
  • Receptors, Interleukin-2 / metabolism
  • Staphylococcal Infections / etiology*
  • Staphylococcal Infections / immunology
  • Staphylococcal Infections / pathology
  • Synovial Membrane / immunology
  • Synovial Membrane / pathology
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / pathology
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / pathology
  • Tumor Necrosis Factor-alpha / metabolism


  • Interleukin-1
  • Receptors, Interleukin-2
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma