Th17-related cytokine profiles in plasma of patients with systemic lupus erythemtosus
10.3760/cma.j.issn.1007-7480.2010.05.015
- VernacularTitle:辅助性T17相关细胞因子在系统性红斑狼疮患者血浆中的变化及意义
- Author:
Fang CHENG
;
Huji XU
;
Dingan YAN
;
Jianping TANG
- Publication Type:Journal Article
- Keywords:
Lupus erythematosus,systemic;
T-Lympholytes,helper-inducer;
Interleukins
- From:
Chinese Journal of Rheumatology
2010;14(5):339-341
- CountryChina
- Language:Chinese
-
Abstract:
Objective To analyze the levels of T helper(Th)17-related cytokines interleukin(IL)-17,IL-22,IL-23 and IL-27 in plasma of patients with systemic lupus erythematosus(SLE).Methods Plasma IL-17,IL-22,IL-23 and IL-27 levels were measured by enzyme-linked immunosorbent assay in 45SLE patients and 32 healthy controls and their associations with each other,disease activity and clinical features were evaluated.Results Plasma levels of IL-17 and IL-23 were significantly higher in SLE patients than in controls[77.8(25.4～487.6)pg/ml vs 36.4(15.7～338.2)pg/ml;14.7(<7.8～247.5) pg/ml vs <7.8(<7.8～81.7)pg/ml.both P<0.01].with no difference between active and inactive disease.In contrast,IL-22 levels were markedly decreased in SLE patients compared with the controls[77.4(<15.6～559.7)pg/ml vs 378.8(21.8～1154.2)pg/ml,P<0.01]and were lower in active disease than in inactive disease(P<0.01).IL-27 levels tended to be higher in SLE patients compared with controls,but the difference was not significant (P>0.05).A strong and positive correlation was found between IL-17 and IL-23 levels(P<0.01)in SLE patients.IL-22 levels were negatively correlated with SLEDAI score,erythrocyte sedimentation rate and antidsDNA antibody titers(all P<0.01),and positively correlated with C3 levels (P<0.05).Each cytokine levels were not related to specific manifestations and treatments.Conclusion Th17 cytokine response in peripheral blood of patients with SLE is abnormal.and IL-17 and IL-22 appear to play different roles in SLE pathophysiology.IL-23/IL-27 imbalance may contribute to the development of Th17-mediated inflammation in SLE.
