Background
Significant progress has been made in understanding the mechanisms of psoriasis, particularly the role of the interleukin (IL)-23/T-helper (Th) 17 axis, leading to novel, targeted therapies. However, many patients develop resistance to treatment over time. Thus, exploring new therapeutic strategies for severe refractory psoriasis remains crucial.
Conclusion
These findings indicate that cladribine can ameliorate imiquimod-induced psoriasiform dermatitis in mice, exhibiting a dose-dependent and sustained therapeutic effect.
Methods
We established an imiquimod (IMQ)-induced psoriasiform dermatitis mouse model to investigate cladribine's effects on skin immune cells. Mice were allocated to five groups: Control, IMQ, High-dose cladribine (30mg/kg), Low-dose cladribine (20mg/kg), and Methotrexate. We assessed cumulative scores, skin pathology, immunohistochemistry, flow cytometry, and serum cytokines. We also studied cladribine's long-term efficacy by reapplying IMQ for a second round (7 days) after five half-lives of cladribine.
Objective
To investigate the effect of cladribine on imiquimod induced psoriasiform dermatitis in mice.
Results
Cladribine significantly ameliorated symptoms and pathological features of IMQ-induced psoriasis in both high and low-dose groups, with efficacy comparable to methotrexate. Cladribine dose-dependently reduced Th17 and Th1 cell frequencies in psoriatic skin, along with associated cytokines. High-dose cladribine demonstrated sustained inhibition of IMQ-induced psoriasis.