Objective To explore the regulatory effect of Cosentyx on skin inflammation and autophagy in psoriasis mice (IMQ-induced) through the C5a / C5aR1 pathway. Methods Twenty-eight 8-week-old BALB/ c male mice were assigned to three groups of nine mice each: Blank, Psoriasis-Model, and Cosentyx-Treated Groups. All except the Blank Group received IMQ and the Cosentyx-Treated Group was treated with Cosentyx (subcutaneous injection, 4. 5 mg / kg twice a day on days 1, 6, and 13). HE staining was used to observe the effect of Cosentyx on pathological damage in the skin of psoriasis mice. ELISA was used to measure the secretion of the proinflammatory cytokines IL-4, IL-8, TNF-α, and IL-1β in psoriasis mouse skin. Spectrophotometry was used to observe the activity of medullary peroxidase (MPO) in mouse skin. Western blot analyses were used to measure Beclin 1 expression and LC3-II/ LC3-I values. Immunohistochemistry analyses were performed to detect the expressions of C5a, C3, C5aR1, and C1qB in skin. Results Cosentyx inhibited the expressions of IL-4, IL-8, TNF-α, IL-1β, and MPO in dermal tissues, improved Beclin 1 expression and the LC3-II/ LC3- I ratio, and downregulated the expressions of C1qB, C3, C5a, and C5aR1. Conclusions Cosentyx inhibited the C5a / C5aR1 pathway, regulated the expression of inflammatory cytokines in psoriasis skin, and slowed psoriasis inflammation. Cosentyx enhanced autophagy in psoriasis skin tissues but we did not determine whether Cosentyx controlled autophagy through the C5a / C5aR1 pathway. Therefore, the mechanism requires further study.