The excellent response of psoriasis to anti-TNF-α(TNF)/IL23/IL17A biologics implies a crucial role for the TNF/IL23/IL17 axis in developing psoriasis. In addition to the TNF/IL23/IL17 axis provided by immune cells, current evidence points to an important contribution of TNF, IL23 and IL17C produced from non-hematopoietic keratinocytes. Therefore, crosstalk between immune cells and keratinocytes forms a multilayered feed-forward loop to accelerate the TNF/IL23/IL17A axis. Many biologics have already been licensed or are under clinical trials. Given that the IL-17 signature is more upregulated in the skin than in synovium in psoriatic arthritis, anti-IL-23/IL-17 agents seem to be superior to anti-TNF-α remedies in the treatment of skin lesions. In this review, we summarize recent topics in psoriasis and the TNF/IL23/IL17 axis.