The protective effect of LCN2 knockout on the imiquimod-induced psoriatic mouse model

LCN2 demonstrates heightened expression levels in psoriasis, providing insight into its potential implication in the development of this inflammatory cutaneous condition. We here report the discovery that LCN2 is an essential molecule involved in the pathogenesis of psoriasis. Deletion of LCN2 in mice resulted in reduced levels of epidermal hyperplasia and inflammatory infiltration in psoriatic skin lesions, as compared to wild-type mice. Hence, our findings suggest that LCN2 may hold promise as a potential therapeutic target for the treatment of psoriasis. To investigate the pathogenic role of LCN2 in a mouse model of psoriasis, we employed LCN2 gene knockout mice for our study.