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IL-33 contributes to disease severity in Psoriasis-like models of mouse

Yaju Duan, Yonghua Dong, Hua Hu, Qiumei Wang, Sheng Guo, Dandan Fu, Xiangfeng Song, Dhan V Kalvakolanu, Zhongwei Tian
Cytokine 2019 March 22, 119: 159-167
Immune cells infiltrating the psoriatic skin secrete high amounts of pro-inflammatory cytokines IL-17, TNF-α, IL-21 and IL-36 resulting in chronic inflammation. However, the exact cellular and molecular mechanisms have not been fully understood. We report here elevation of IL-33 expression in psoriatic lesions. Studies in imiquimod (IMQ)-induced mice with psoriatic inflammation confirmed a critical role for IL-33 in driving the disease. IL-33 reduces the CD4+ and CD8+ cells, inhibits autophagy in IMQ-treated mouse skin, and promoted tyrosyl phosphorylation of STAT3. Thus, IL-33 appears to be a major risk factor for severity of psoriasis-like skin inflammation. Our findings may open new perspectives for understanding the mechanisms and developing a therapeutic strategy for psoriasis.


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