IL‐18 is involved in the pathogenesis of atopic dermatitis, psoriasis, and allergic contact dermatitis. CXCL9, CXCL10, and CXCL11 recruit type 1 T cells, and the production of these chemokines by keratinocytes is enhanced in these dermatoses. We examined the in vitro effects of IL‐18 on IFN‐γ‐induced CXCL9, CXCL10, and CXCL11 production in human keratinocytes. IL‐18 enhanced the IFN‐γ‐induced secretion and mRNA expression of CXCL9, CXCL10, and CXCL11 in parallel to the activation of NF‐κB, STAT1, and IFN‐regulatory factor (IRF)‐1. Antisense oligonucleotides against NF‐κB p50, p65, or STAT1 suppressed CXCL9, CXCL10, and CXCL11 production, and antisense IRF‐1 suppressed CXCL11 production. Inhibitors of PI3 K, p38 MAPK, and MEK suppressed IL‐18 plus IFN‐γ‐induced CXCL9, CXCL10, and CXCL11 production and NF‐κB, STAT1, and IRF‐1 activities. IL‐18 induced phosphorylation of ERK and Akt, while IFN‐γ induced phosphorylation of p38 MAPK. These results suggest that IL‐18 may potentiate IFN‐γ‐induced CXCL9, CXCL10, and CXCL11 production in keratinocytes by activating NF‐κB, STAT1, or IRF‐1 through PI3 K/Akt and MEK/ERK pathways. These effects of IL‐18 may promote the infiltration of type 1 T cells into lesions with inflammatory dermatoses and amplify the skin inflammation. IL‐18 may act as a pro‐inflammatory cytokine in these dermatoses and thus is a candidate therapeutic target.