BIPHASIC CONTROL OF NF-κB ACTIVATION INDUCED BY THE TRIGGERING OF HLA-DR ANTIGENS EXPRESSED ON B CELLS

The regulation of NF-κB activation following the triggering of HLA-DR antigens by mAb L243 has been studied at various time in Raji cells. Electrophoretic mobility shift assays demonstrated a strong increase of NF-κB DNA binding after triggering of HLA-DR antigens. Using TNF-α-activity neutralizing antibodies, the authors demonstrated that the upregulation of NF-κB was found to depend, at later time point, on an autocrine effect of TNF-α secreted following triggering of HLA-DR antigens. In contrast, it was found to be TNF-α independent in the early time point. Moreover, the upregulation of NF-κB 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-1 or staphylococcal enterotoxin B, regulate the NF-κB binding activity.