We now identify keratinocytes, as well as dermal fibroblasts, as cells that can upregulate a number of chemoattractive and proinflammatory factors that are associated with AD and psoriasis in response to TWEAK, and that TWEAK can also synergize with signals from IL-17A or IL-13 to further upregulate some of these molecules. The gene discussed is TNFSF12; the disease is psoriasis.