Interleukin-17A (IL-17) is an immune cell-derived cytokine that acts on various types of cells, including epidermal keratinocytes, and induces production of antimicrobial peptides and cytokines to induce antibacterial and antifungal responses. An excess of this IL-17 action leads to inflammatory skin disease like psoriasis. Recently, we demonstrated that IκB-ζ, a nuclear IκB protein that modulates NF-κB-dependent transcription, is IL-17-inducibe and mediates IL-17-induced responses. However, the mechanism controlling IκB-ζ expression in IL-17-stimulated cells remained unclear. Here, we found that a JAK kinase TYK2 positively regulates IL-17-induced IκB-ζ expression in keratinocytes using TYK2 siRNA. In addition, TYK2 knockdown reduced IL-17-induced expression of IκB-ζ target genes (IL19, DEFB4A and CSF3). Production of IL-19 protein from IL-17A-stiumulated keratinocytes was also reduced by TYK2 knockdown. Luciferase assays revealed that overexpression of wild-type TYK2, but not kinase-inactive TYK2 (K930R), enhances IκB-ζ promoter activity independently of IL-17, and that IL-17 stimulation, but not TYK2 overexpression, post-transcriptionally stabilizes IκB-ζ mRNA via its 3’-untranslated region. IL-17 signaling counteracted Regnase-1-mediated mRNA degradation. Western blotting and chromatin immunoprecipitation experiments showed that STAT3, a transcription factor and substrate of TYK2, is constitutively phosphorylated and binds to IκB-ζ promoter in keratinocytes. Similarly to TYK2, STAT3 knockdown suppressed IL-17-induced expression of IκB-ζ mRNA, although neither TYK2 nor STAT3 were activated by IL-17. A JAK inhibitor cerdulatinib reduced the levels of tyrosine phosphorylation and IκB-ζ promoter association of STAT3, and IL-17-induced IκB-ζ upregulation. Importantly, in the imiquimod-induced skin inflammation model, TYK2-deficient mice showed reduced inflammation and concomitant reduction of IκB-ζ mRNA compared to wild-type mice. These results suggest that, although TYK2 is not directly involved in IL-17-induced post-transcriptional stabilization of IκB-ζ mRNA, constitutive activity of TYK2-STAT3 pathway acts as pivotal factor for the basal transcription level of IκB-ζ, thereby determining the magnitude of IL-17-induced skin inflammation.