Relationship between the Apoptosis of MNCS and the Expression of Cytokines and Adhesion Molecules in Patients with SLE
- VernacularTitle:细胞因子、黏附分子对SLE患儿MNCS凋亡的影响
- Author:
Jianqiang SHI
;
Zhonglu YE
;
Ding LI
- Publication Type:Journal Article
- Keywords:
SLE;
Apoptosis;
Cytokines, MNCS
- From:
Journal of Chinese Physician
2001;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore relationship between the changes of mononuclear cells (MNCS) apoptosis and the levels of inflammatory cytokines and adhesion molecules in patients with systemic lupus erythematosus(SLE). Methods The apoptotic rates of MNCS in 32 patients with SLE and 10 healthy subjects were detected with flow cytometry, and the plasma levels of inflammatory cytokines(IL-8, IL-6,TNF-? and NO) and adhesion molecules(P-Sel, ICAM-1) were assayed with ELISA. Results The percentage of MNCS apoptosis in the patients with active stage of SLE was obviously higher than that in healthy subjects and patients with remission stage of SLE, and there was no significant difference in the percentage of MNCS apoptosis between healthy subjects and patients with remission stage of SLE. The levels of plasma IL-8, TNF-?, IL-6, NO, P-sel and ICAM-1 in patients with active stage of SLE were significantly higher than those in healthy subjects and the patients with remission stage of SLE, and were positively correlated with the percentage of MNCS apoptosis and the severity of SLE.There was no significant difference in the levels of plasma inflammatory cytokines and adhesion molecules between patients with remission stage of SLE and healthy subjects. Conclusion The apoptotic rate of MNCS increased in the patients with active SLE, and was closely associated with the severity and efficacy of SLE. The high expressions of inflammatory cytokines and adhesion molecules may be the reason of MNCS apoptotic increase. Appropriately regulating the expression of cytokines and adhesion molecules, and moderately controlling the apoptosis of MNCS may improve the prognosis of SLE.