Stem cells of the dendritic cell lineage in the liver : demonstration and analysis

1.肝移植后不久，移植物来源的dc具有非常不成熟的表型，TcR- Ig- MHCI+ MHCII+ ICAM1+ CD11b- CD11c- αEβ7整合素-和CD86-，通过宿主淋巴组织的HEV和脾边缘窦进行弥漫性转运。这些dc与宿主T细胞聚集在一起，开始大量的宿主增殖反应。此外，具有浆细胞样DC表型的MHCII+ Ig- B220+细胞和MHCII+ TcR+细胞以及MHCII- T细胞和Ig+ B细胞同时以与小鼠模型相似的方式进行迁移（参考文献3,7）。骨髓DC部分在静脉转移后转移到宿主淋巴组织，而肝脏粗DC部分则没有，这可能是因为包括酶消化在内的分离过程造成了细胞损伤。手术前7天的耐受性诱导方案供体特异性输血（DST）完全阻断了这种转移，并显著抑制了宿主T细胞的增殖反应。DST方案本身在宿主脾脏诱导抗体形成细胞反应，导致供体特异性IgM和IgG_1细胞毒性同种抗体的产生。这导致血液中迁移的供体细胞迅速消失。由于小鼠肝移植后肝内T细胞凋亡的报道，我们认为在宿主淋巴组织中没有产生效应T细胞的肝内致敏可能导致T细胞反应流产。这种缺失可能超过同种异体反应性T细胞的产生，导致肝脏手术耐受。同源供体大鼠肝移植后供体细胞可存活2年。DC型较少。

1.Soon after the liver transplantation, graft-derived DCs with a very immature phenotype, TcR- Ig- MHCI+ MHCII+ ICAM1+ CD11b- CD11c- αEβ7 integrin- and CD86-, performed a diffuse transmigration through the HEV and splenic marginal sinus of host lymphoid tissues. These DCs clustered with host T cells where a massive host proliferative response started.2.In addition, MHCII+ Ig- B220+ cells with plasmacytoid DC phenotype and MHCII+ TcR+ cells as well as MHCII- T cells and Ig+ B cells concomitantly transmigrated in a similar fashion as the mice model (ref 3, 7).3&6.While the bone marrow DC fraction transmigrated to host lymphoid tissues after i.v. transfer, the liver crude DC fraction did not, probably because the isolation procedure including enzymal digestion caused cell injury.4.The tolerance-inducing regimen, donor-specific transfusion (DST) 7 d before operation completely blocked this transmigration and considerably suppressed the proliferative response of host T cells there. The DST regimen itself induced antibody forming-cell response in the host spleen, leading to donor-specific IgM and IgG_1 cytotoxic alloantibody production. This caused a rapid elimination of migrating donor cells in the blood. Since intragraft T cell apoptosis is reported after the murine liver transplantation, we consider that the intrahepatic sensitization without effector T cell production in the host lymphoid tissues may induce the abortive T cell response. The deletion may exceed the production of alloreactive T cells, resulting in the liver operational tolerance.5.The donor cells persisted up to 2 years after liver transplantation from the congeneic donor rats. Few of them bore DC phenotype.