Anti-interleukin 33 treatment alleviates psoriatic dermatitis in mice induced imiquimod

Interleukin-33(IL-33), is constitutively expressed in the epithelial cells of the skin. It has been reported that IL33 contributed to the severity of the disease in psoriasis-like mouse models. In the current study, we evaluated the effect of anti-IL-33 antibody (Ab) in imiquimod-induced psoriatic dermatitis in mice. Our observations showed that anti-IL-33 Ab ameliorated the erythema, scaling, epidermal thickness and spleen index. Additionally, we found anti-IL-33 Ab significantly decreased the expression of psoriasis-related cytokines. Moreover, antiIL-33 Ab significantly reduced Ki-67 positive cells, CD3+CD4+T cells, and CD3+CD8+T cells in the skin lesions. Furthermore, anti-IL-33 Ab treatment down-regulated the expression of phosphorylation of STAT3 and IL-33 in model mouse. These results indicated that the anti-IL-33 Ab alleviated the seriousness of skin lesions, inhibited the activation of the STAT3, lymphocyte infiltration and the secretion of pro-inflammatory cytokines in imiquimod-induced psoriatic dermatitis in mice, suggesting IL-33 may be a therapeutic target for the treatment of psoriasis.

Automated summary

In this study, the effect of anti-IL-33 antibody was evaluated in a mouse model of psoriatic dermatitis. The results showed that anti-IL-33 antibody improved the symptoms of the disease and reduced the expression of psoriasis-related cytokines. Furthermore, treatment with anti-IL-33 antibody inhibited the activation of STAT3 and reduced lymphocyte infiltration in the skin lesions, suggesting IL-33 as a potential therapeutic target for psoriasis treatment.