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The murine pre-B cell line 70Z/3 responds to lipopolysaccharide by up-regulating the surface expression of kappa (kappa) light chain through activation of the transcription factor NF kappa B. Interleukin-4 (IL-4), a T cell cytokine, is a known inhibitor of some LPS-mediated events. We investigated whether IL-4 could inhibit the up-regulation of kappa light chain and activation of NF kappa B by LPS in 70Z/3. IL-4 partially inhibited both the LPS-induced expression of kappa light chain and also the activation of NF kappa B as judged by an NF kappa B reporter gene assay. Additionally, electrophoretic mobility shift assays confirmed this effect on LPS-induced NF kappa B DNA binding activity in the nucleus. Surprisingly, proteolytic degradation of I kappa B alpha (MAD3), a prerequisite for NF kappa B activation, was unaffected by IL-4, implying that this cytokine inhibits some subsequent undefined event in the activation of NF kappa B. IL-4 was also found partially to inhibit NF kappa B activity induced by tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1 beta). These results indicate that there may be a common mechanism for the well-documented anti-inflammatory effects of IL-4 and that this mechanism involves the transcription factor NF kappa B.

Original publication




Journal article


Eur J Immunol

Publication Date





2961 - 2966


Animals, Antigens, CD, B-Lymphocytes, Base Sequence, Cell Line, DNA, DNA-Binding Proteins, Depression, Chemical, Gene Expression Regulation, Genes, Immunoglobulin, Genes, Reporter, Hematopoietic Stem Cells, I-kappa B Proteins, Immunoglobulin M, Immunoglobulin kappa-Chains, Interleukin-1, Interleukin-4, Lipopolysaccharides, Mice, Molecular Sequence Data, NF-KappaB Inhibitor alpha, NF-kappa B, Promoter Regions, Genetic, Receptors, Antigen, B-Cell, Receptors, Tumor Necrosis Factor, Receptors, Tumor Necrosis Factor, Type I, Tumor Necrosis Factor-alpha, beta-Galactosidase