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NKT細胞在誘導小鼠門靜脈耐受中的作用
來源: | 作者: | 發布時間:2014-4-15 17:06:13

NKT細胞在誘導小鼠門靜脈耐受中的作用
李卓男1,關連越1,劉宏宇1,辛敏剛2,王展鵬1,葉研碩1,付佩堯1,李巍1
基金項目:基金項目:國家自然科學基金(81170416; 81273264); 教育部博士點基金(20100061110069);吉林省科技廳國際合作基金(2011742);天普研究基金(01201046);吉林省自然科學基金(201015178) 作者簡介:李卓男(1987年生),男,經治醫師,器官移植與免疫耐受 通信聯系人:李。1963年生),女,教授,器官移植與免疫耐受.

(1. 吉林大學中日聯誼醫院肝膽胰外科,長春,130033; 2. 吉林大學中日聯誼醫院麻醉科,長春,130033)
摘要:目的:明確NKT細胞在介導門靜脈耐受中的作用。方法:利用小鼠同種異體異位心臟移植模型,移植前經門靜脈注入同種異體脾細胞誘導心臟移植物免疫耐受,經尾靜脈注入同種異體脾細胞組設為對照,觀察兩組心臟移植物存活情況,應用流式細胞術方法監測肝臟非實質細胞的亞型的變化,應用免疫組化等方法分析淋巴細胞免疫功能。結果:同種異體抗原經門靜脈注入后肝臟中NKT細胞數量明顯增加,并表達的較高的PD-L1水平,同時CD4+CD25+Foxp3+調節性T細胞(Treg)在受體肝臟及脾內均明顯增加,并表達較高的CTLA4、PD-1和PD-L1分子。心臟移植物存活時間在經門靜脈注入同種異體抗原的實驗組受體鼠內明顯延長。結論:NKT細胞在誘導門脈免疫耐受中起重要作用,經門靜脈注入同種異體抗原能夠誘導肝臟內NKT擴增,繼而誘導受體鼠肝及脾內CD4+ CD25+ Foxp3+ Treg15 細胞擴增,顯著延長同種異體心臟移植物存活時間。
關鍵詞:NKT細胞;調節性T細胞;小鼠;心臟移植;門脈耐受
中圖分類號:R392.4
Effects of NKT cells on portal tolerance induction
Li zhuonan1, Guan lianyue1, Liu hongyu1, Xin mingang2, Wang zhanpeng1, Ye yanshuo1, Fu peiyao1, Li wei1
(1. Dept of Hepatobiliary-pancreatic Surgery,China-Japan Union Hospital of Jilin University,Changchun,130033; 2. Anesthesiology,China-Japan union hospital of Jilin University,Changchun,130033)

Abstract: Aim: to explore the role of NKT cells on portal tolerance induction. Method: allogeneic mouse heterotopic heart transplantation model was employed. Allogeneic spleen cells was injected through the portal vein before heart transplantation, the spleen cells injected through the tail vein was used as control. Heart allograft survival was followed and the phenotypes of liver nonparenchymal cells were characterized by flowcytometry. The cytokine profiles of host lymphocytes were detected by  immunohistochemistry. Results: liver NKT cells was increased significantly after receiving the allogeneic spleen cells through portal vein, rather than tail vein injection. PD-L1 level were also increased on NKT cells. CD4+CD25+Foxp3+ regulatory T (Treg) cells were increased too in the livers and spleens of the mice who received alloantigen injection through portal vein. Those Treg expressed high CTLA4, PD1 and PD-L1 molecules on their surface. The heart allograft survival time was significantly prolonged in the mice who received alloantigen through portal vein injection. Conclusion: NKT cells plays an important role on portal tolerance induction. Alloantigen delivery through the portal vein results in NKT cells expansion in the liver and CD4+CD25+Foxp3+ Treg expansion in both livers and spleens, and further prolongs the heart allograft survival.
Key words: NKT cells;Treg cells;mouse;heart transplantation;portal tolerance

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