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Activation of NF‐κB may be necessary but is not sufficient for induction of H‐2 antigens by TNF in J558L murine myeloma cells
Author(s) -
Wolchok Jedd D.,
Goodman Adam R.,
Vilçek Jan
Publication year - 1994
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.55.1.7
Subject(s) - tumor necrosis factor alpha , nf κb , lipopolysaccharide , nfkb1 , antigen , p50 , biology , microbiology and biotechnology , transcription factor , electrophoretic mobility shift assay , traf2 , inflammation , immunology , biochemistry , gene , tumor necrosis factor receptor
We have investigated the role of the transcription factor NF‐ κ B in the induction of H‐2 antigens by tumor necrosis factor (TNF) in murine J558L myeloma cells. An earlier report suggested that J558L cells may have a defect in NF‐ κ B activation in response to some stimuli. Treatment of J558L cells with either TNF or lipopolysaccharide (LPS) resulted in nuclear translocation of NF‐ κ B, as demonstrated by electrophoretic mobility shift assay. Both TNF and LPS activated the same NF‐ κ B nuclear complexes, composed of the p50 and p65 subunits. LPS mediated a stronger and more sustained activation of NF‐ κ B than TNF. In contrast, TNF induced higher levels of H‐2 antigen surface expression than did LPS, suggesting that activation of NF‐ κ B is not sufficient for optimal enhancement of H‐2 expression. An inhibitor of NF‐ κ B activation, pyrrolidinedithiocarbamate (PDTC), dramatically reduced the induction of H‐2 antigen by TNF, supporting the view that NF‐ κ B is required for TNF‐induced H‐2 antigen expression. Constitutive levels of H‐2 antigen expression on the cell surface and of nuclear NF‐ κ B also decreased after PDTC treatment. However, PDTC had a smaller inhibitory effect on LPS‐induced NF‐ κ B activation and H‐2 antigen expression, suggesting that TNF and LPS activate NF‐ κ B by somewhat different pathways. J. Leukoc. Biol . 55: 7–12; 1994.