IL-33 contributes to disease severity in Psoriasis-like models of mouse. (July 2019)

• Record Type: Journal Article
• Authors: Duan, Yaju; Dong, Yonghua; Hu, Hua; Wang, Qiumei; Guo, Sheng; Fu, Dandan; Song, Xiangfeng; Kalvakolanu, Dhan V.; Tian, Zhongwei
• Is Part Of: Cytokine. Volume 119(2019)
• Page Start: 159
• Page End: 167
• Publication Date: 2019-07
• Subjects: Interleukin-33 -- HaCaT cell -- Autophagy -- Psoriasis-like skin inflammation -- STAT3; Cytokines -- Periodicals; 571.844
• DOI: 10.1016/j.cyto.2019.02.019
• Languages: English
• ISSNs: 1043-4666

Abstract

Abstract: 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.