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Activation of gene transcription by IL-4, IL-13 and IFN-gamma through a shared DNA binding motif
I Köhler1, P Alliger, E P Rieber
1Institute for Immunology, Ludwig-Maximilians-University, München, Germany.
Both interleukin-4 (IL-4) and interleukin-13 (IL-13) induce the transcription factor NF-IL4 (nuclear factor IL-4) which preexists in an inactive form and binds to an IL-4 responsive element (IL-4RE) in the promoter regions of IL-4/IL-13-dependent genes. UV-crosslinking and SDS gel electrophoresis indicate that NF-IL4 consists of at least two DNA-binding components of 50 kDa and 100-130 kDa. The IL-4 responsive element is also recognized by an interferon-gamma (IFN-gamma)-induced DNA binding protein for which a Mr of 50 kDa has been determined. A common DNA binding motif for different transcription factors might provide the basis for the frequently observed functional antagonism between IL-4/IL-13 and IFN-gamma. The activation of transcription factors by IL-4/IL-13 and IFN-gamma could be blocked by inhibitors of tyrosine kinases and ser/thr phosphatases but not by a PKC inhibitor, suggesting related signal transduction pathways for these cytokines.
Both interleukin-4 (IL-4) and interleukin-13 (IL-13) induce the transcription factor NF-IL4 (nuclear factor IL-4) which preexists in an inactive form and binds to an IL-4 responsive element (IL-4RE) in the promoter regions of IL-4/IL-13-dependent genes. UV-crosslinking and SDS gel electrophoresis indicate that NF-IL4 consists of at least two DNA-binding components of 50 kDa and 100-130 kDa. The IL-4 responsive element is also recognized by an interferon-gamma (IFN-gamma)-induced DNA binding protein for which a Mr of 50 kDa has been determined. A common DNA binding motif for different transcription factors might provide the basis for the frequently observed functional antagonism between IL-4/IL-13 and IFN-gamma. The activation of transcription factors by IL-4/IL-13 and IFN-gamma could be blocked by inhibitors of tyrosine kinases and ser/thr phosphatases but not by a PKC inhibitor, suggesting related signal transduction pathways for these cytokines.