中文摘要：

目的探讨CD4＋T细胞免疫应答在小鼠抗GBM肾小球肾炎中的作用。方法将C57BL/6小鼠随机分为肾炎模型组和正常对照组,两组均给予兔IgG预致敏,10 d后肾炎模型组给予兔抗GBM血清（0.2 mL/20 g）尾静脉注射,正常对照组给予正常兔血清,分别于第7、14、21、28天行以下处理：收集尿和血清样本检测血肌酐（Scr）、血尿素氮（BUN）和尿蛋白/尿肌酐（UmAlb/c）的含量;光镜和电镜观察肾组织病理学改变;流式细胞仪检测淋巴器官和肾脏局部免疫细胞分布情况;Real-time PCR检测肾组织中IFN-γ、IL-4、IL-17A、TGF-β1、CCL-2、CCL-4、CCL-5和CXCL-1等细胞因子mRNA的含量;ELISA检测血清中IFN-γ、IL-4、IL-17A、IL-12、IL-10和TGF-β1等细胞因子的表达水平。结果与正常对照组小鼠相比,肾炎模型组小鼠的Scr、BUN和UmAlb/c均明显升高（P〈0.05）;光镜下可见典型新月体肾炎样病理改变,免疫荧光可见兔IgG和鼠IgG沿GBM呈线性沉积;小鼠脾脏中Th1、Th2、Th17和Treg细胞比例明显增加,同时肾脏局部有大量Th1、Th2和Th17细胞浸润;血清及肾脏局部IFN-γ、IL-4、IL-17A和TGF-β1等细胞因子表达水平相应上调。结论 CD4＋T细胞免疫应答能介导小鼠抗GBM肾小球肾炎并在其病理进程中发挥促进作用。

英文摘要：

[Objective] To investigate the effect of CD4＊T cell-mediated immune response in mice anti- GBM glomerulonephritis. [Methods] C57BL/6 mice were randomly divided into nephritic group and normal control group. All mice were preimmunized by rabbit IgG. 10 days later, the mice in nephritic group were injected with rabbit auti-GBM serum （0.2 mL/20 g） and the mice in normal control group were injected with normal rabbit serum. All the mice were observed for Scr, BUN and UmAlb/c at the 7th day, the 14th day, the 21st day and the 28th day, respectively. At the same time, the kidneys were collected for the observation of the pathological changes. Flow cytometry was used to detect the infiltration of immune cells in lymphoid organs and renal tissues. The mRNA of IFN-γ IL-4, IL-17A, TGF-β1, CCL-2, CCL-4, CCL-5 and CXCL- 1 in kidney were detected by Real-time PCR and the level of serum IFN-γ IL-4, IL-17A, IL-12, IL-10 and TGF-β1 were determined by ELISA. [Results] Compared with those in control group, Scr, BUN and U- mAlb/c of mice raised obviously in anti-GBM nephritis model （P 〈0.05）. Typical pathological changes of cres- centic nephritis could be seen in the model mice. Immunofluorescence examination showed that rabbit IgG and mouse IgG linearly deposited along the GBM. Then the distribution of immunologic cells in spleen showed that Thl, Th2, Th17 and Treg cells increased in nephritic group; the infiltration of Thl, Th2 and Thl7 in kidneys were also increased in nephritic group. The expression of IFN-γ, IL-4, IL-17A and TGF-β1 in kidney and serum were also up-regulated in nephritic group. [Conclusion] CD4＋ T cell-mediated immune response can contribute to anti-GBM glomerulonephritis in mice and play an important promotion in the progress of pathology.