The correlation between STAT3 phosphorylation and the activity of Behcet's disease
10.3969/j.issn.1672-8467.2018.02.005
- VernacularTitle:STAT3磷酸化与白塞病临床活动性的关系
- Author:
Hua-Fang BAO
1
;
Jian-Fei CAI
;
Yong CHEN
;
Dan LUO
;
Yan SHEN
;
Jun ZOU
;
Jian-Long GUAN
Author Information
1. 复旦大学附属华东医院免疫风湿科 上海200040
- Keywords:
Behcet's disease;
signal transducer and activator of transcription 3;
pathogenesis;
TH1 cell;
Th17 cell;
Stattic
- From:
Fudan University Journal of Medical Sciences
2018;45(2):169-176
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role of signal transducer and activator of transcription 3 (STAT3) phosphorylation in the pathogenesis of Behcet's disease (BD),and to investigate the association between STAT3 phosphorylation and disease activity in BD patients.Methods Peripheral blood mononuclear cell (PBMC) was isolated from 15 mL peripheral boood of 10 active BD patients (BD-A),10 BD patients in remission (BD-R) and 10 healthy controls (HC) respectively.The blockade of STAT3 phosphorylation was performed by Stattic.The PBMC was divided into Stattic subgroup (treated with 2.5 μmol/L stattic and 1 640 medium,5 mL) and blank control subgroup (treated with 5 mL 1 640 medium),respectively.The protein levels of phosphorylated STAT3 (pSTAT3) and STAT3 were examined by flow cytometry and Western blot.The protein and mRNA levels of TNF-α,IFN-γ and IL-17 were tested by RT-PCR and ELISA.Two-way ANOVA and Bonferroni post hoc test were used to analyze the results.Results Compared with HC,the BD patients showed higher protein levels of pSTAT3 and STAT3,and higher protein and mRNA levels of TNF-α,IFN-γ and IL-17;compared with blank control subgroup,the protein levels of pSTAT3 and STAT3,and protein and mRNA levels of TNF-α,IFN-γ and IL-17 decreased in Stattic subgroup.In the BD-A group,the protein level of pSTAT3,and protein and mRNA levels of TNF-α,IFN-γ and IL-17 were significantly higher than those in the BD-R group.Conclusions An increased activation of the STAT3 pathway may contribute to the pathogenesis of BD and relate to disease activity in BD patients by inducing TH1 and Th17 cells activation.
