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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。
Objective: To investigate the immune mechanism of T helper cells (Th) related cytokines in the pathogenesis of lupus nephritis. Methods: Sixty-four patients with systemic lupus erythematosus (SLE) and 28 healthy controls were enrolled in this study. Serum levels of IL-17, IFN-γ and IL-4 were measured by enzyme-linked immunosorbent assay (ELISA) Its correlation with SLEDAI, SDI, 24-hour urinary protein was studied. Results: The level of serum IL-17 in lupus nephritis group was significantly higher than that in lupus nephritis group and healthy control group (P <0.001), and the level of IFN-γ in lupus nephritis group was significantly higher than that in lupus nephritis group (P <0.05) (P <0.01). Serum IL-4 level was significantly higher in lupus nephritis group and non-nephritis group than in healthy control group (P <0.01). The ratio of IFN-γ / IL-4 in lupus nephritis group was significantly higher than that in lupus nephritis group (P <0.01) and healthy control group (P <0.05) Control group (P <0.01). The level of serum IFN-γ in patients with SLE was positively correlated with SLEDAI score (r = 0.402, P <0.05). The levels of serum IL-17 and IL-4 were positively correlated with SLEDAI, SDI, anti-dsDNA antibody, C3,24 hour urinary protein No correlation between quantity. CONCLUSION: The levels of IL-17, IFN-γ, IL-4 and other proinflammatory cytokines in peripheral blood of patients with lupus nephritis all increase to different extents to promote inflammation and tissue damage, and are involved in the immune pathogenesis of lupus nephritis.