Act1 expression and its possible regulatory mechanisms in Sj(o)gren's syndrome
10.3760/cma.j.issn.1007-7480.2014.05.002
- VernacularTitle:核因子-κB激活剂1在干燥综合征中的表达及其调节机制的探讨
- Author:
Xiaohui ZHANG
;
Wei ZHOU
;
Juan GUO
;
Juan ZHAO
;
Zhuoli ZHANG
- Publication Type:Journal Article
- Keywords:
Sj(o)gren's syndrome;
Interleukin-17;
Act1
- From:
Chinese Journal of Rheumatology
2014;18(5):292-296,后插1
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the nuclear factor-kappa-B activator 1 (Act1) expression in salivary gland and peripheral blood lymphocytes in patients with Sj(o)gren's syndrome (SS),and to explore its possible regulatory mechanisms.Methods The Act1 expression in salivary gland tissue from 10 patients with SS was analyzed by immunohistochemical staining,and immunolluorescence double staining was used to detect Act1-expressing cells.Peripheral blood mononuclear cells were obtained from 28 SS patients and 22 healthy controls (HC).The Act1 expression in different lymphocyte subpopulations was determined by flow cytometry and Act1-mRNA expression was detected by reverse transcription polymerase chain reaction (RT-PCR),and the data was analyzed by Wilcoxon test and Mann-Whitney U test and Pearson correlation analysis.Results Remarkable expression of Actl in the salivary glands from SS patients was observed,especially in T lymphocytes,in contrast to the few expression in B lymphocytes.The expression of Act1 in the peripheral CD4+ T cells,CD8+ T cells,CD20+ B cells was higher in SS patients than HC.There was no significant difference of Act 1-mRNA levels in peripheral blood mononuclear cells in healthy controls and SS patients.However,a tendency of up-regulation of Act1 expression was noticed in SS patients than healthy controls (0.84±0.35 vs 0.79±0.21,U=274.5,P＞0.05),and the up-regulation of Act1 was also found in those SS patients with hypergammaglobulinemia (0.88±0.39 vs 0.75±0.27,U=73.0,P＞0.05) or with internal organ involvement(0.92±0.38 vs 0.77±0.33,U=75.0,P＞0.05),but the differences were not statistically significant.Conclusion Our data suggest that Act1 may be involved in the pathogenesis of SS by negative feedback mechanism in B cell-mediated humoral immune pathway,and positive feedback mechanism in IL-17 mediated T-cell immune pathways.Act1 may be associated with disease activity and severity in SS.
