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[文摘发布]依赖于IL-10的迟发性免疫抑制可诱导肝
Author:Yang ZF, Ngai P, Lau CK, Ho DW, Tam KH, Lam CT, Poon RT, Fan ST
Source:Liver Transpl. 2007 Apr;13(4):571-8.
IF:4.447(2005)
This study aims to investigate the potential role of endogenous interleukin (IL)-10 in long-term liver allograft survival induced by delayed immunosuppression (FK506 days 2-7). Liver transplantation was performed by using Dark Agouti and Lewis rats as donors and recipients, respectively. The delayed immunosuppression protocol induced indefinite allograft survival. A transient upregulation of plasma IL-10 levels was detected in the nontreatment and FK506 treatment groups. Macrophages were found to be one of the major sources of IL-10 produced from the liver allografts. Administration of IL-10-neutralizing antibody shortened the long-term isograft survival and FK506-induced indefinite allograft survival, particularly in the FK506 group. Damaged liver graft histology and increase of plasma alanine aminotransferase levels were detected in the groups with IL-10 antibody treatment. In an ex vivo setting, IL-10 recombinant protein augmented the expression of Foxp3, downregulated the expression of IL-2 and interferon gamma, and induced the generation of CD4(+)CD25(+)Foxp3(+) and CD8(+)CD25(+)Foxp3(+) cells, but this effect was blocked by the administration of IL-10 antibody. Finally, administration of IL-10 recombinant protein after the decline of endogenous IL-10 levels improved allograft survival, and a 100% long-term allograft survival was achieved by the combination of IL-10 with low-dose FK506. In conclusion, the delayed immunosuppression could induce long-term liver allograft survival in the presence of endogenous IL-10 produced by the tissue macrophages. Supplementary exogenous IL-10 administration combined with low-dose immunosuppressive drug may be a useful strategy to induce long-term liver allograft survival.
个人以为L-10只是众多耐受信号中的一员而已,在其信号途径的上游或下游还有许多耐受分子参与.本文作者又提供多一份此类设想的证明. 本人认领此文。如在48小时内未能提交译文，其他战友可自由认领。 Title nduction of long-term liver allograft survival by delayed immunosuppression is dependent on interleukin-10.
题目：依赖于IL-10的迟发性免疫抑制可诱导移植肝长期生存
Author:Yang ZF, Ngai P, Lau CK, Ho DW, Tam KH, Lam CT, Poon RT, Fan ST
Source:Liver Transpl. 2007 Apr;13(4):571-8.
IF:4.447(2005)
This study aims to investigate the potential role of endogenous interleukin (IL)-10 in long-term liver allograft survival induced by delayed immunosuppression (FK506 days 2-7). Liver transplantation was performed by using Dark Agouti and Lewis rats as donors and recipients, respectively. The delayed immunosuppression protocol induced indefinite allograft survival. A transient upregulation of plasma IL-10 levels was detected in the nontreatment and FK506 treatment groups. Macrophages were found to be one of the major sources of IL-10 produced from the liver allografts. Administration of IL-10-neutralizing antibody shortened the long-term isograft survival and FK506-induced indefinite allograft survival, particularly in the FK506 group. Damaged liver graft histology and increase of plasma alanine aminotransferase levels were detected in the groups with IL-10 antibody treatment. In an ex vivo setting, IL-10 recombinant protein augmented the expression of Foxp3, downregulated the expression of IL-2 and interferon gamma, and induced the generation of CD4(+)CD25(+)Foxp3(+) and CD8(+)CD25(+)Foxp3(+) cells, but this effect was blocked by the administration of IL-10 antibody. Finally, administration of IL-10 recombinant protein after the decline of endogenous IL-10 levels improved allograft survival, and a 100% long-term allograft survival was achieved by the combination of IL-10 with low-dose FK506. In conclusion, the delayed immunosuppression could induce long-term liver allograft survival in the presence of endogenous IL-10 produced by the tissue macrophages. Supplementary exogenous IL-10 administration combined with low-dose immunosuppressive drug may be a useful strategy to induce long-term liver allograft survival.
本文的目的是研究内源性IL-10在迟发性免疫抑制所诱导的同种异体移植肝长期存活中的可能作用(FK506 days 2-7)。使用Dark Agouti鼠（DA鼠）和路易（Lewis）鼠分别作为供体和受体进行肝移植。迟发性免疫抑制实验诱导同种异体移植肝的不定期存活。在未治疗组和他克莫司（FK506）治疗组可以观察到一个暂时性血浆IL-10水平升高。可以发现巨噬细胞是移植肝产生IL-10的一个主要来源。给予IL-10中和抗体会缩短同基因移植肝所应有的长期存活率，更会缩短他克莫司治疗的同种异体移植肝的不定期存活率。在IL-10抗体处理组中能观察到移植肝的组织损伤和血浆丙氨酸氨基转移酶水平升高。在离体实验中，IL-10重组蛋白能增加Foxp3的表达，减少IL-2和γ－干扰素的表达，诱导CD4(+)CD25(+)Foxp3(+) 和 CD8(+)CD25(+)Foxp3(+)的细胞增殖，而这些作用能够被IL-10抗体封闭。在内源性IL-10水平下降以后，给予IL-10重组蛋白能增加同种异体移植肝的存活率，联合给予IL-10和低剂量他克莫司能够使同基因移植肝100%长期存活。总之，在组织巨噬细胞产生的内源性IL-10存在时，迟发性免疫抑制能诱导同种异体移植肝长期存活。补充外源性IL-10并联合应用低剂量免疫抑制药物方案对同种异体移植肝长期存活是有用的。 编译格式还是不太合适，参看一下我签名档里的文摘类新闻编译格式帖。
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作者:admin@医学,生命科学 2010-10-25 17:11
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