Mouse liver transplantation tolerance: the role of hepatocytes and nonparenchymal cells.
Mouse liver transplantation tolerance: the role of hepatocytes and nonparenchymal cells.
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发表时间：
1995
影响因子：
0.9
通讯作者：
N. Thai;S. Qian;F. Fu;Y. Li;H. Sun;A. Demetris;R. Duquesnoy;T. Starzl;J. Fung
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文献类型：
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作者：
N. Thai;S. Qian;F. Fu;Y. Li;H. Sun;A. Demetris;R. Duquesnoy;T. Starzl;J. Fung
在许多品系组合中，包括那些跨越主要和次要组织不相容性屏障的品系组合，小鼠原位肝移植物在没有免疫抑制的情况下被自发接受。此外，肝脏移植物的接受，导致供体特异性接受后续的皮肤或心脏移植物。尽管肝移植耐受（LGT）的确切机制尚未完全了解，但LGT已被归因于：（1）供体非实质细胞（NPC）迁移导致随后的受体/供体血淋巴细胞毒症1，2;和（2）可溶性MHC分子的肝细胞（HC）释放。3我们使用了一种实验模型，原理上类似于Rapaport等人的模型，Sriwatanawongsa等人5以前使用过，通过构建嵌合供体肝脏（其NPC已被同种异体骨髓移植（BMT）替代）来测试NPC或HC是否是LGT中更重要的组分。
Mouse orthotopic liver allografts are spontaneously accepted without immunosuppression in many strain combinations including those crossing major and minor histoincompatibility barriers. Liver allograft acceptance, moreover, leads to donor-specific acceptance of subsequent skin or heart allografts. Although the precise mechanisms of liver graft tolerance (LGT) are not completely understood, LGT has been attributed to: (1) donor nonparenchymal cell (NPC) migration leading to subsequent recipient/donor hematolymphoid chirnerism1,2; and (2) hepatocyte (HC) release of soluble MHC molecules.3 We have used an experimental model, similar in principle to that of Rapaport et al,4 and used previously by Sriwatanawongsa et al5 to test whether the NPC or HC was the more important component in LGT by constructing chimeric donor livers whose NPC have been replaced by allogeneic bone marrow transplantation (BMT).