文章摘要
邢倩1 苏厚恒1 崔佳佳1 李光文1 王斌2.Th 细胞因子IL-17、IFN-γ、IL-4 在狼疮性肾炎中的表达及意义[J].,2012,12(8):1537-1540
Th 细胞因子IL-17、IFN-γ、IL-4 在狼疮性肾炎中的表达及意义
Role of Peripheral Blood Th Cells Relevant Cytokines in Patientswith Lupus Nephritis
  
DOI:
中文关键词: 系统性  红斑狼疮  IL-17  IFN-γ  IL-4
英文关键词: Systemic  Lupus erythematosus  IL-17  IFN-γ  IL-4
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作者单位
邢倩1 苏厚恒1 崔佳佳1 李光文1 王斌2 青岛市市立医院免疫风湿科 
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中文摘要:
      目的:探讨T 辅助细胞(Th)相关细胞因子在狼疮性肾炎发病中的免疫机制作用。方法:64 例系统性红斑狼疮患者和28 例 健康体检者作为对照,采用酶联免疫吸附测定法(ELISA 法)检测所有受试者血清IL-17、IFN-γ、IL-4 水平,并对其与SLEDAI、 SDI、24 小时尿蛋白量相关性进行研究。结果:狼疮性肾炎组血清IL-17 水平显著高于狼疮无肾炎组和健康对照组(P<0.001),狼 疮性肾炎组血清IFN-γ 水平显著高于狼疮无肾炎组(P<0.05)和健康对照组(P<0.01),血清IL-4 水平在狼疮性肾炎组、狼疮无肾炎 组均显著高于健康对照组(P<0.01)。狼疮性肾炎组IFN-γ/IL-4 比值显著高于狼疮无肾炎组(P<0.01)和健康对照组(P<0.05);狼疮 无肾炎组IFN-γ/IL-4 比值显著低于健康对照组(P<0.01)。SLE 患者血清IFN-γ 表达水平与SLEDAI 积分呈正相关(r =0.402, P <0.05),血清IL-17、IL-4 表达水平与SLEDAI、SDI、抗ds-DNA 抗体、C3、24 小时尿蛋白量均无相关性。结论:狼疮性肾炎患者外 周血中IL-17、IFN-γ、IL-4 等促炎细胞因子均有不同程度升高促起炎症发生及组织损伤,参与了狼疮性肾炎的免疫发病过程。
英文摘要:
      Objective: To investigate the effect and the clinical significance of Th cells in the pathogenesis of patients with lupus nephritis (LN). Methods:64 systemic lupus erythematosus patients and 28 healthy controls were enrolled. The concentrations of serum IL-17, IFN-γ, IL-4 were measured by enzyme-linked immunosorbent assay (ELISA). Results: 1. The expression of IL-17 in LN Group exhibited a significant increase compared with that in SLE Group and healthy controls (P<0.001). 2. The levels of IFN-γ in LN Group were higher than those in SLE Group and in healthy controls (P<0.05, P<0.01, respectively). 3. The levels of IL-4 in SLE Group, LN Group were higher than those in healthy controls (P<0.01). 4. Th1/Th2 (IFN-γ/IL-4) ratio in LN Group increased significantly than that in SLE Group (P<0.01) and HC group (P<0.05); Th1/Th2 (IFN-γ/IL-4) ratio decreased in SLE Group compared with that in HC group (P<0. 01). 5. The levels of IFN-γ were positively correlated with SLEDAI scores in SLE patients (P<0.05). Conclusions: The significantly elevated serum IL-17, IFN-γ, IL-4 levels in lupus nephritis, suggesting that Th17/ Th1/ Th2 functional imbalance may be involved in the pathogenesis of renal damage in SLE patients.
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