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机构地区:[1]北京农学院动物科学技术系,北京102206 [2]中国科学院动物研究所生物膜与膜生物工程国家重点实验室,北京100101
出 处:《中国实验动物学报》2010年第1期9-12,I0003,共5页Acta Laboratorium Animalis Scientia Sinica
基 金:国家自然科学基金重点项目(No.30630060);北京市教委资助项目(KM200910020006)
摘 要:目的通过小鼠骨髓细胞剔除Smad3基因,观察小鼠病理变化以及免疫T细胞状态。方法将Smad3基因剔除Smad3-/-)的小鼠骨髓细胞和野生型(Smad3+/+)小鼠骨髓细胞分别移植给60Co射线照射GFP小鼠。观察骨髓移植后GFP小鼠体征变化,第6周处死小鼠,取肠道固定,HE染色观察其病理变化,流式细胞技术检测淋巴结中T细胞变化。结果移植Smad3-/-骨髓细胞的GFP小鼠逐渐消瘦,大肠出现炎症;淋巴结中活化型的CD4+CD62LloT细胞增多。结论骨髓细胞TGF-β信号受阻,可导致小鼠患炎症疾病,引起免疫T细胞活化。Objective To investigate the changes of T cells and disease development in the mice with Smad3 deficiency in the bone marrow cells.Methods Bone marrow cells obtained from Smad3 null(Smad3^-/-) mice and wild type(Smad3^+/+) mice were injected to Co^60-irradiated GFP mice,respectively.The general states of the bone marrow recipients were observed.The mice were sacrificed at the sixth week and the histopathological changes in the intestines were examined.The changes of T cells from lymph nodes were detected by flow cytometry.Results Smad3^-/- bone marrow recipient mice appeared a wasting syndrome and intestinal inflammation.The amount of CD4^+CD62L^lo T cells in lymph nodes was significantly increased.Conclusion These results indicate that the mice with Smad3 deficiency in the bone marrow cells present an inflammatory disorder and their T cells are activated.
关 键 词:Smad3基因剔除- 骨髓细胞 T细胞活化 移植
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