趋化因子及其受体介导的细胞迁移与移植物抗宿主病  

Chemokines and Chemokine Receptors Induced Lymphocyte Migration and Graft-versus-host Disease

作　　者：曹琦[1] 张雁云[1] 

机构地区：[1]上海交通大学医学院,上海市免疫学研究所,上海200025

出　　处：《细胞生物学杂志》2006年第6期808-812,共5页Chinese Journal of Cell Biology

摘　　要：移植物抗宿主病(graft-versus-hostdisease,GVHD)是同种异基因骨髓移植中的重要并发征。供者T细胞在输注入受者体内后迁移进入淋巴组织,识别受者同种异基因抗原,被受者抗原递呈细胞(antigenpresentingcell,APC)激活,进而活化、增殖分化,介导急性GVHD的发生。现有的研究已表明,活化的异体效应性T细胞经淋巴组织迁移进入黏膜组织以及实质性靶器官,如消化道、肝脏、肺脏和皮肤,进而造成这些器官和组织的损伤。因此,分子间相互作用尤其是趋化因子及其受体介导的效应性细胞的迁移是GVHD发生发展过程中关键的一环,受到了广泛的关注。进一步以趋化因子及其受体为靶标,亦可能形成有效的免疫生物学治疗,具有广阔的应用前景。Graft-versus-host disease （GVHD） is a significant complication of allogeneic bone marrow transplantation （allo-BMT）. Acute GVHD is mediated by effector donor T cells, which migrate to lymphoid tissues soon after transplantation, recognize host allo-antigens, and become activated by host antigen presenting cells （APCs）. Recent studies on GVHD suggest that activated effector allo-T cells from lymphoid tissues migrate into target organs such as the gastro-intestinal （GI） tract, liver, lung, and skin and cause tissue damage. Moreover, accumulating documents indicated that the migration of effector allo-T cells was mediated by chemokines and chemokine receptors. Involvement of the interaction between chemokine/chemokine receptor would develop an efficient target for GVHD therapy. It would provide a novel insight into developing therapeutic strategy for GVHD.

关 键 词：趋化因子及趋化因子受体 异体效应性T细胞迁移 移植物抗宿主病 

分 类 号：R392[医药卫生—免疫学]