The clinical significance of AT-rich interaction domain 3a+ B cell change in patients with systemic lupus erythematosus
10.3760/cma.j.issn.1007-7480.2019.11.005
- VernacularTitle: 系统性红斑狼疮患者腺嘌呤-胸腺嘧啶碱基富含互作域3a+B细胞的变化及临床意义
- Author:
Yunxia YAN
1
;
Xiaojun TANG
;
Wenchao LI
;
Lingyun SUN
Author Information
1. Department of Rheumatology and Immunology, the Drum Tower Clinical Medical School of Nanjing Medical University, Jiangsu 210008, China
- Publication Type:Clinical Trail
- Keywords:
Lupus erythematosus, systemic;
Lupus nephritis;
B cells;
AT-rich interaction domain 3a
- From:
Chinese Journal of Rheumatology
2019;23(11):742-746,C11-1
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression of transcription factor AT-rich interaction domain 3a (ARID3a) in peripheral blood B cells of patients with systemic lupus erythematosus (SLE) and its clinical significance.
Methods:Peripheral blood mononuclear cells were isolated from 17 SLE patients and 13 healthy controls. Then, the expression of ARID3a by B cells was determined by flow cytometry. Data was analyzed with independent sample t test. The correlations between the frequencies of ARID3a+ B cells and clinical indicators of SLE patients were assessed by Pearson cor relation analysis. The expression of ARID3a in kidney was detected by immunohistochemistry in 14 cases of lupus nephritis (LN).
Results:The percentages of ARID3a+ B cells in SLE patients [(51.6±3.2)%] were significantly higher than those in healthy controls [(32.6±3.4)%](t=4.0, P<0.01). There was a positive correlation between the percentages of ARID3a+ B cells in SLE patients and their 24-hour urinary protein (r=0.68, P<0.05). Furthermore, the percentages of ARID3a+ B cells in peripheral blood from patients with active LN[(62.3±4.3)%] were remarkably higher than that from patients without LN or with inactive LN [(43.3±2.8)%] (t=3.8, P<0.01). The expression of ARID3a in glomerula and tubules of LN patients markedly increased.
Conclusion:Elevated expression of transcription factor ARID3a in B cells may participate in the pathogenesis of LN.
