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

被引:31
作者
Duan, Yaju [1 ]
Dong, Yonghua [1 ]
Hu, Hua [1 ]
Wang, Qiumei [2 ]
Guo, Sheng [3 ,4 ]
Fu, Dandan [1 ]
Song, Xiangfeng [3 ,4 ]
Kalvakolanu, Dhan V. [5 ]
Tian, Zhongwei [1 ]
机构
[1] Xinxiang Med Univ, Affiliated Hosp 1, Dept Dermatol, 88 Jiankang Rd, Xinxiang 453000, Henan, Peoples R China
[2] Cent Hosp Xinxiang, Dept Dermatol, Xinxiang 453000, Henan, Peoples R China
[3] Xinxiang Med Univ, Sch Basic Med Sci, Inst Precis Med, Xinxiang 453000, Henan, Peoples R China
[4] Xinxiang Med Univ, Dept Immunol, Xinxiang 453000, Henan, Peoples R China
[5] Univ Maryland, Sch Med, Dept Microbiol & Immunol, Baltimore, MD 21201 USA
基金
芬兰科学院;
关键词
Interleukin-33; HaCaT cell; Autophagy; Psoriasis-like skin inflammation; STAT3; MAST-CELL; AUTOPHAGY; INTERLEUKIN-33; KERATINOCYTES; INFLAMMATION; MECHANISMS; EXPRESSION; ARTHRITIS; CYTOKINE; BECLIN;
D O I
10.1016/j.cyto.2019.02.019
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Immune cells infiltrating the psoriatic skin secrete high amounts of pro-inflammatory cytokines IL-17, TNF-alpha, 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.
引用
收藏
页码:159 / 167
页数:9
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