Biphasic control of NF-kappa B activation induced by the triggering of HLA-DR antigens expressed on B cells

Cytokine. 1997 May;9(5):295-9. doi: 10.1006/cyto.1996.0168.

Abstract

The regulation of NF-kappa B activation following the triggering of HLA-DR antigens by mAb L243 has been studied at various times in Raji cells. Electrophoretic mobility shift assays demonstrated a strong increase of NF-kappa B DNA binding after triggering of HLA-DR antigens. Using TNF-alpha-activity neutralizing antibodies, the authors demonstrated that the upregulation of NF-kappa B was found to depend, at later time point, on an autocrine effect of TNF-alpha secreted following triggering of HLA-DR antigens. In contrast, it was found to be TNF-alpha independent in the early time point. Moreover, the upregulation of NF-kappa B binding activity is regulated by the triggering of selected epitopes of HLA-DR antigens. In fact, mAb L243 but not the staphylococcal superantigens, staphylococcal exotoxin toxic shock syndrome toxin-I or staphylococcal enterotoxin B, regulate the NF-kappa B binding activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibodies, Monoclonal / immunology
  • B-Lymphocytes / cytology
  • B-Lymphocytes / immunology*
  • HLA-DR Antigens / immunology*
  • Humans
  • NF-kappa B / immunology
  • NF-kappa B / metabolism*
  • NF-kappa B p50 Subunit
  • Proto-Oncogene Proteins / immunology
  • Proto-Oncogene Proteins c-rel
  • Transcription Factor RelA
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Antibodies, Monoclonal
  • HLA-DR Antigens
  • NF-kappa B
  • NF-kappa B p50 Subunit
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-rel
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha