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机构地区:[1]解放军第一五二医院,河南平顶山市467000 [2]第三军医大学西南肝胆外科医院
出 处:《中华普通外科杂志》2004年第6期355-357,共3页Chinese Journal of General Surgery
摘 要:目的探讨联合应用体外培养供体特异性不成熟树突状细胞及环胞素A(CsA)对受体体内Th1 /Th2淋巴细胞分化的影响。方法建立大鼠同种异体原位肝移植模型 ,88只LWE大鼠和SD大鼠随机分为 3组 :(1 )对照组 :术后不予免疫抑制剂 ;(2 )CsA组 :术后第 2天起隔日腹腔内按1mg/ 1 0 0 g 体重注射CsA ,共 3次 ;(3)CsA +DC组 :除术后按CsA组腹腔注射CsA外 ,第 8天阴茎背静脉注射 1 0 6个供体骨髓体外培养的不成熟树突状细胞 (DCim)。术后观察各组的生存时限及 5、1 0、1 5、2 5d分别取标本行肝脏免疫病理学检查、腹腔淋巴结中INF γmRNA、IL 6mRNA含量的检测。结果CsA +DC组的生存时限为 (2 7 0± 1 0 )d ,较对照组及CsA组显著延长 (P <0 0 5 ) ;CsA +DC组受体腹腔淋巴结中的INF γmRNA含量较对照组及CsA组低 (P <0 0 5 ) ,而IL 6mRNA含量则较前两组升高 (P <0 0 5 )。结论联合应用环孢素A和体外培养的供体特异性DCim后受体体内Th2型淋巴细胞含量升高 ,而Th1型淋巴细胞含量降低 ;通过调节受体体内Th1Objective To investigate the effect of donor specific immature dendritic cells infusion in combination with CsA on differentiation of liver recipient′s Th1/Th2 cell in rats. Methods Allograft models of orthotopic rat liver transplantation were established, 88 LEW rats (recipient) and SD rats (donor) were randomly divided into three groups: (1) in control group no immunosuppresive drug was used after liver transplantation. (2) in CsA group 1 mg/100 g body weight of CsA was injected intraperitoneally every the other day for 3 times beginning the 2nd day after liver transplantation. (3) in CsA+DC group additional 1× 10 6 immature DC from donor bone marrow was injected through penile vein at the 8th day after operation, in combination with CsA as in CsA group. Rats were sacrificed for immunopathological examination and detection of INF γmRNA, IL 6 mRNA of celiac lymph node on 5th, 10th, 15th, and 25th day after transplantation. Results The average recipient survival time in the CsA+DC group was (27 0±1 0) days, significantly longer than that in control and CsA group (all P <0 05); INF γmRNA level in CsA+DC group was lower than that in other groups, whereas IL 6 mRNA level in CsA+DC group was the highest ( P < 0 05). Conclusions Donor specific immature DCs in combination with CsA inhibits the recipient′s immunological rejection.
关 键 词:特异性不成熟树突状细胞 环胞素A 环胞素A受体 Th1/Th2淋巴细胞 细胞分化 肝移植 免疫排斥反应
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