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The purpose of this study was to uncover the mechanism of tumor necrosis factor (TNF)-α induction by fibroblast growth factor-7 (FGF-7) in human HaCaT cells and the potential role of FGF-7ospecific antibody F-9 in psoriatic therapy.TNF-α expression in HaCaT cells induced by FGF-7 was analyzed by quantitative polymerase chain reaction,weste blot analysis,and enzyme-linked immunosorbent assays.In vivo,the BALB/c mouse psoriasis model established by topical application of imiquimod (IMQ) was used to determine the role of FGF-7-specific antibody (F-9) in skin inflammation.We found that induction of TNF-α expression by FGF-7 in HaCaT cells was suppressed by FGF-7-specific antibody F-9.Weste blot analysis results showed that FGF-7 induced TNF-α expression in HaCaT cells via the FGF receptor 2 (FGFR2)/AKT/NF-κB signaling pathway.In vivo,F-9 could significantly ameliorate the inflammations in a mouse psoriatic model evaluated by Psoriasis Area and Severity Index scores and ear thickness,which was consistent with the results of hematoxylin-eosin staining,immunohistochemistry assay,and weste blot analysis.These results indicate that FGF-7 induces TNF-cα expression in HaCaT cells and FGF-7 antibody F-9 alleviates IMQ-induced psoriasiform in mice.Therefore,FGF-7/FGFR2 signaling pathway is a potential target for psoriasis treatment.