组织工程与重建外科杂志
組織工程與重建外科雜誌
조직공정여중건외과잡지
JOURNAL OF TISSUE ENGINEERING AND RECONSTRUCTIVE SURGERY
2010年
3期
121-127
,共7页
李红%郭子宽%李秀森%江小霞%朱恒%要辉宇%王晓燕%苏永丰%廖丽%刘元林%吴英%张毅%毛宁
李紅%郭子寬%李秀森%江小霞%硃恆%要輝宇%王曉燕%囌永豐%廖麗%劉元林%吳英%張毅%毛寧
리홍%곽자관%리수삼%강소하%주항%요휘우%왕효연%소영봉%료려%류원림%오영%장의%모저
急性移植物抗宿主病%抗原呈递细胞%免疫调节%体内间充质干细胞%T淋巴细胞
急性移植物抗宿主病%抗原呈遞細胞%免疫調節%體內間充質榦細胞%T淋巴細胞
급성이식물항숙주병%항원정체세포%면역조절%체내간충질간세포%T림파세포
Acute Graft-versus-Host Disease%Antigen presenting cells%Immunoregulation%In vivo mesenchymal stem cells%T lymphocyte
目的 研究间充质干细胞的体内免疫调节活性.方法 将C57/BL脾脏细胞输注入受亚致死量照射的BALB/c小鼠,建立急性移植物抗宿主病模型,受体小鼠或同时接受密质骨骨髓来源的间充质干细胞,流式细胞技术检测脾细胞表面表达的活性分子.结果 模型经输注间充质干细胞后,鼠脾脏CD11b+细胞表达的CD86和CD69减少,提示抗原呈递细胞的成熟度下降.此外,作为一种效应T细胞早期活化和发育的标记,CD3+CD69+细胞/CD3+细胞的比值降低,导致脾内CD3+细胞的绝对和相对数目减少.但是,在同系脾细胞输注模型中,CD11b+细胞表面的CD69和MHCⅡ表达以及CD3+细胞表面的CD69不受影响.结论 MSCs可以分3个阶段抑制急性移植物抗宿主病,有望成为急性移植物抗宿主病的有效治疗手段,但仍需进行深入研究.
目的 研究間充質榦細胞的體內免疫調節活性.方法 將C57/BL脾髒細胞輸註入受亞緻死量照射的BALB/c小鼠,建立急性移植物抗宿主病模型,受體小鼠或同時接受密質骨骨髓來源的間充質榦細胞,流式細胞技術檢測脾細胞錶麵錶達的活性分子.結果 模型經輸註間充質榦細胞後,鼠脾髒CD11b+細胞錶達的CD86和CD69減少,提示抗原呈遞細胞的成熟度下降.此外,作為一種效應T細胞早期活化和髮育的標記,CD3+CD69+細胞/CD3+細胞的比值降低,導緻脾內CD3+細胞的絕對和相對數目減少.但是,在同繫脾細胞輸註模型中,CD11b+細胞錶麵的CD69和MHCⅡ錶達以及CD3+細胞錶麵的CD69不受影響.結論 MSCs可以分3箇階段抑製急性移植物抗宿主病,有望成為急性移植物抗宿主病的有效治療手段,但仍需進行深入研究.
목적 연구간충질간세포적체내면역조절활성.방법 장C57/BL비장세포수주입수아치사량조사적BALB/c소서,건립급성이식물항숙주병모형,수체소서혹동시접수밀질골골수래원적간충질간세포,류식세포기술검측비세포표면표체적활성분자.결과 모형경수주간충질간세포후,서비장CD11b+세포표체적CD86화CD69감소,제시항원정체세포적성숙도하강.차외,작위일충효응T세포조기활화화발육적표기,CD3+CD69+세포/CD3+세포적비치강저,도치비내CD3+세포적절대화상대수목감소.단시,재동계비세포수주모형중,CD11b+세포표면적CD69화MHCⅡ표체이급CD3+세포표면적CD69불수영향.결론 MSCs가이분3개계단억제급성이식물항숙주병,유망성위급성이식물항숙주병적유효치료수단,단잉수진행심입연구.
Objective To investigate the in vivo immunoregulatory activities of mesenchymal stem cells (MSCs). Methods A murine aGvHD model was developed by transfusion of C57/BL splenocytes, with or without compact bone-derived MSCs, into sublethally irradiated BALB/c mice. The phenotypic features of the splenocytes were analyzed by flow cytometry after transplantation. Results MSCs infusion decreased the expression of CD86 and CD69 molecules on splenic CDllb+ cells of aGvHD mice, suggesting of the decreased maturation of antigen presenting cells. Meanwhile, the ratio of CD3+ CD69+ to CD3+ cells, a parameter for early activation and effector T cell formation, was dramatically down-regulated, resulting in the enhancement of the absolute and relative number of splenic CD3+ cells by MSCs co-transfer. However, the expression level of MHCⅡ and CD69 on CD11b+ cells and CD69 on CD3+ cells were not affected in the syno-splenocyte infusion model. Conclusion The results here suggest that MSCs can inhibit aGvHD at the three development stages of specific cytotoxic T lymphocytes. Further investigations are needed for designing better strategies to manipulate aGvHD in clinical settings.
