• Home
  • Search Results
  • IL-33 contributes to disease severity in Psoriasis-like models of mouse.

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

Cytokine (2019-03-27)
Yaju Duan, Yonghua Dong, Hua Hu, Qiumei Wang, Sheng Guo, Dandan Fu, Xiangfeng Song, Dhan V Kalvakolanu, Zhongwei Tian
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.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Monoclonal Anti-β-Actin antibody produced in mouse, clone AC-15, ascites fluid
Sigma-Aldrich
Anti-ST2 antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
Anti-IL-33 antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution