Interleukin‐4 inhibits χ light chain expression and NFχB activation but not IχBα degradation in 70Z/3 murine pre‐B cells

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Abstract
The murine pre‐B cell line 70Z/3 responds to lipopolysaccharide by upregulating the surface expression of kappa (χ) light chain through activation of the transcription factor NFχB. 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 χ light chain and activation of NFχB by LPS in 70Z/3. IL‐4 partially inhibited both the LPS‐induced expression of χ light chain and also the activation of NFχB as judged by an NFχB reporter gene assay. Additionally, electrophoretic mobility shift assays confirmed this effect on LPS‐induced NFχB DNA binding activity in the nucleus. Surprisingly, proteolytic degradation of IχBα (MAD3), a prerequisite for NFχB activation, was unaffected by IL‐4, implying that this cytokine inhibits some subsequent undefined event in the activation of NFχB. IL‐4 was also found partially to inhibit NFχB activity induced by tumor necrosis factor‐alpha (TNF‐α) and interleukin‐1‐beta (IL‐1β). 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 NFχB.