Overview of the signalling leading to induction of ELF3 and subsequent upregulation of expression of proinflammatory factors. First, TNF stimulation leads to NF-κB-mediated transcriptional activation of NFKBIZ. Robust expression of IκBζ protein requires additionally stabilization of NFKBIZ mRNA, which occurs following binding of IL-17A to its cell surface receptor. Secondly, IκBζ protein associates with DNA-bound NF-κB and C/EBPβ transcription factors to induce expression of secondary response genes, including ELF3. Third, ELF3 induces the expression of a variety of proinflammatory factors by functioning in collaboration with NF-κB and AP-1. The model is simplified to show only main signalling events. AP-1: activator protein-1; C/EBPβ: CCAAT/enhancer-binding protein-β; ELF3: E74-like factor-3; IκBζ: NF-κB inhibitor-ζ; NF-κB: nuclear factor-κB; NFKBIZ: gene encoding IκBζ.