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目的 :将本室建立的用活化淋巴细胞诱导的系统性红斑狼疮 (SLE)样小鼠模型与国际上公认的用慢性GVHR诱导的SLE样小鼠模型进行比较 ,进一步探索SLE的发病机理。方法 :分别将亲代Balb c小鼠淋巴细胞经静脉和用ConA活化的(Balb c×C5 7BL 6 )F1代小鼠淋巴细胞经皮下途径输入F1代小鼠 ,用ELISA测定IgG类抗dsDNA抗体和抗组蛋白抗体 ,用免疫荧光法检测抗核抗体 (ANA)荧光核型和肾小球内免疫复合物沉积 ,用免疫印迹法检测抗可溶性核抗原 (ENA)抗体。结果 :亲代淋巴细胞免疫F1代小鼠所致的慢性GVHR和活化F1代小鼠淋巴细胞均可诱导F1代小鼠产生高滴度的抗dsDNA抗体、抗组蛋白抗体等ANA ,并且肾脏都有明显的IgG类免疫复合物沉积。但亲代淋巴细胞免疫组ANA核型以颗粒型、核仁型为主 ,ENA多肽谱多在 32、47、6 7kD处显色 ;而活化淋巴细胞免疫组以胞浆型、周边型、均质型为主 ,ENA多肽谱在 2 8、47、6 7kD处显色。结论 :这 2种方法均可诱导出SLE样综合征 ,但其抗核抗体谱有所不同。
OBJECTIVE: To further investigate the pathogenesis of SLE by comparing the established SLE mouse model induced by activated lymphocytes and the internationally recognized SLE mouse model induced by chronic GVHR. Methods: The F1 generation mice were injected subcutaneously with lymphocytes of Balb c mouse lymphocytes (Balb c × C5 7BL 6) which were activated by ConA and Balb c mice respectively. The IgG anti-dsDNA antibody and Anti-histone antibodies were detected by immunofluorescence staining of anti-nuclear antibody (ANA) fluorescent karyotype and glomerular immune complex deposition, Western blot detection of anti-soluble nuclear antigen (ENA) antibody. RESULTS: Chronic GVHR induced by F1 generation of parental lymphocytes and lymphocytes activated by F1 generation all induced high titer anti-dsDNA antibody, anti-histone antibody and other ANA in F1 generation mice, and the kidneys had Clear IgG immune complex deposition. However, the ANA karyotype of the parental lymphocyte immunization group was mainly granular type and nucleolar type, and the spectrum of ENA peptide was mostly at 32, 47, 67 kD. The activated lymphocyte immunization group was cytoplasm type, peripheral type, homogeneity Type, ENA peptide profiles at 28,47,6 7kD color. Conclusion: Both SLE-like syndromes can be induced by these two methods, but the anti-nuclear antibody spectrum is different.