大鼠肝再移植模型的建立

目的 为研究肝移植免疫机制建立新的实验途径。方法 选用近交系LEW、WF大鼠，在第1次肝移植后的第3天，把移植肝取出，重新植入到另一个宿主内，两次移植均采用了双套管法的原位全肝移植术式。结果 经过了40例的再移植训练后，后期19例的1周生存率达73．7％。在LEW→WF→WF组合中，经再移植后宿主未出现排斥反应且自然长期生存。结论 精巧、熟练的外科手术技术是保障再移植成功的关键。移植肝的免疫原性在术后早期基本上消失了。     

调节性CD4+T细胞在大鼠自发肝移植耐受中的作用

目的 探讨在肝移植的自发耐受模型中，调节性CD4^＋T细胞的免疫抑制作用机制。方法 利用近交系大鼠从Lewis（LEW）到Wistar Furth（WF）的肝移植组合，对移植后不同时期的宿主注射抗CD4的单克隆抗体（Anti-CD4mAb），然后抽血检测丙氨酸氨基转氨酶（ALT）的动态变化；并结合细胞毒性T淋巴细胞（CTL）试验了解宿主脾细胞中T细胞亚群的动态改变。结果 对肝移植自然生存的宿主注射Afiti—CD4mAb后，术后第21天、42天均能够诱导出肝损害（排斥反应），但第56天、100天以上的则未能诱导出来，且该损害能被抗CD8单克隆抗体阻断。另外CTL试验显示宿主的脾细胞中，初始型CTL前体细胞在移植56d后未能检测出来。结论 在自发性肝耐受模型中。宿主术后早期存在由CD4^＋T细胞介导的下调原始效应性T细胞的作用机制。     

大鼠原位肝移植术后腹腔细菌感染对移植物免疫排斥反应的影响

目的探讨大鼠原位肝移植术后腹腔细菌感染对移植肝排斥反应的影响。方法采用成年雄性DA、Lewis大鼠(上海斯莱克实验动物有限责任公司)为供受体建立大鼠原位肝移植模型, 采用随机数字表分组法分成4组, G1为LEW到LEW, 同基因对照组;G2为LEW到LEW, 同基因腹腔感染组;G3为DA到LEW, 异基因对照组;G4为DA到LEW, 异基因腹腔感染组。每组于术后第2、4、6、8天4个时间点(每个时间点4只)收集标本, 通过观察移植肝病理表现、细胞凋亡, 评估移植肝排斥反应的不同表现。组间比较采用单因素方差分析, 病理等级资料采用秩和检验。结果苏木精-伊红(HE)显示, 感染后第5天(术后第8天), G3组RAI高于G4组(8.0±0.8比6.5±1.3, χ2=12.711, P<0.05)。感染后5 d(术后第8天)G4组移植肝实质及汇管区凋亡细胞指数(AI)高于G3组[(28.53±5.27)%比(17.33±4.99)%, F=32.298, P<0.05]。结论大鼠肝移植术后腹腔细菌感染诱导移植肝汇管区及小叶中央静脉周围浸润淋巴细胞凋亡增多, 导致移植肝排斥反应减轻...     

预输注供者凋亡的脾细胞诱导大鼠肝移植免疫耐受的研究

目的探讨肝移植预输注地塞米松体内诱导凋亡的供体脾细胞诱导受体肝移植免疫耐受可能性。方法实验分5组,对照组,单纯供体地塞米松处理组,单纯输供者脾细胞组,地塞米松诱导供者凋亡脾细胞输注组,第三品系组。每组均做Wistar至SD的肝移植,每组各10只Wistar、SD大鼠。用地塞米松3mg/(kg·d)处理Wistar大鼠3d后,第4天取供体的脾细胞输注受体,第10天行大鼠肝移植。观察术后第7天肝功能(ALT、TBil)的变化、病理改变和受体生存期。结果肝移植预输注凋亡细胞组的ALT、TBil较其它各组显著低(P<0·05);生存期明显长(P<0·05),病理改变较轻。结论肝移植预输注地塞米松体内诱导供体凋亡的脾细胞能诱导受体大鼠对移植肝的免疫耐受。     

基因重组融合蛋白B7-CD28共刺激阻断剂对大鼠移植肾存活的影响

目的观察基因重组融合蛋白B7-CD28共刺激阻断剂CTLA-4Ig对大鼠移植肾存活的影响.方法肾移植术后第2天每只用药组大鼠腹腔内注射CTLA-4Ig0.5mg,观察移植肾存活时间;术后第20天,测定受体对供体及无关大鼠的单向混合淋巴细胞反应(MLR),并观察移植肾病理改变.结果与对照组相比,用药组移植肾存活时间显著延长[(42.6±6.4)d,(8.2±1.2)d,P＜0.001)].术后第20天,用药组移植肾仅有散在淋巴细胞浸润;受体对供体的MLR明显低于正常对照[(5832±674)cpm、(13486±2166)cpm,P＜0.001)],而受体对无关大鼠的MLR与正常对照相比无显著差异(P＞0.05).结论CTLA-4Ig通过诱导受体对供体抗原特异性的免疫反应低下状态明显延长了大鼠移植肾存活时间.     

大黄素对大鼠移植肝细胞凋亡的作用

目的探讨大黄素对大鼠肝脏移植术后肝细胞凋亡的作用。方法建立大鼠肝移植模型,分为三组:对照组,供受体均为LEW大鼠;移植组;供体为LEW大鼠,受体为BN大鼠;大黄素组,在移植组基础上,移植术后每日以大黄素50mg·kg-1腹腔注射。分别于术后第1,3,5,7天各取6只移植大鼠的肝脏,TUNEL法染色,检测肝脏细胞凋亡。以肝脏细胞凋亡阳性细胞数占总肝脏细胞数的百分比作为肝细胞凋亡指数(AI)。结果移植组肝细胞于术后第1天即已出现凋亡,第3天明显增加,第7天达到高峰。大黄素组各时间点肝细胞凋亡指数明显小于对应的移植组(P<0.01)。结论大黄素对肝移植急性排斥反应中肝细胞凋亡有显著抑制作用。     

二种大鼠供肝原位肝移植术后近期死因的分析

目的　分析大鼠正常心跳供体 (HBD)和心跳停搏供体 (NHBD)原位肝移植术后近期死因的异同。方法　雄性SD大鼠随机分成HBD和NHBD两组 ;NHBD组又分别设心跳停搏 30min(NHBD 30 )和 45min(NHBD 45 )两组。每组各行原位肝移植 5 0、30和 30次。结果　HBD和NHBD组冷缺血、无肝期、IVC阻断、受体手术时间分别为 6 9 76± 1 5 2和 70 32± 1 5 3min、16 46± 0 96和 16 40± 0 73min、2 2 5 6± 1 73和 2 2 75± 1 16min、89 38± 3 75和 90 5 8± 3 76min ;HBD组术后近期 (1周 )共有 5只受体分别死于原发性移植肝无功能 (1)、麻醉过深 (1)、肺部感染 (2 )和SVC吻合口漏 (1) ;而NHBD组术后近期共有 36只受体分别死于原发性移植肝无功能 (17)、麻醉过深 (4)、无肝期较长 (3)和供肝再灌注后渗血 (12 )。结论　二种供体原位肝移植术后的近期死因确实存在着差异。     

肝移植大鼠肝窦内皮细胞的损伤及PGE1对其的保护作用

目的　探讨肝移植大鼠术后早期肝窦内皮细胞功能的改变及前列腺素E1(PGE1)对其的保护作用。方法　用“两袖套法”建立大鼠原位肝移植模型 ,其中A组为正常大鼠空白对照组 ,B组为正常大鼠供体肝移植手术对照组 ,C组为休克性大鼠供体肝移植实验对照组 ,D组为PGE1保护的休克性大鼠供体肝移植实验组 ,每组各 8只。肝移植各组 (无特别说明均指受体 )于术后 6h取血 ,检测其血清中的肝脏酶学 (ALT、LDH )、丙二醛 (MDA)和一氧化氮 (NO) ,以及血浆内皮素 (ET)水平 ,并取肝组织作常规病理学检查 ,比较各组有无差异。结果　各移植组供肝冷保存时间及无肝期均接近 ,分别为 (2± 0 .5 )h和 (15± 3 )min ;B、D组术后 6h全部存活 ,存活率 10 0 % ;C组术后 6h存活 5只 ,存活率 62 .5 %。与C组比较 ,D组ALT、LDH、MDA、ET明显降低 (P<0 .0 5 ) ,NO明显升高 (P<0 .0 5 )。C组肝脏病理学检查发现有明显的组织学损害 ,而B、D组肝脏组织结构基本完好。结论　肝移植可造成肝窦内皮细胞明显损害 ,血清NO和血浆ET水平可较好地反映肝窦内皮细胞的功能状态。PGE1通过稳定血流动力学和稳定肝窦内皮细胞质膜 ,可减轻移植肝肝窦内皮细胞的损害。     

补体激活参与脑死亡诱导的供肝损伤及移植后级联损伤

目的验证补体激活是否参与脑死亡诱导的供肝损伤及移植后级联损伤。方法收集2017年1月到2020年10月在广西医科大学第一附属医院行肝移植治疗儿童患者的临床资料、血清和肝组织样本, 包括脑死亡供体肝移植患者26例和活体供肝肝移植患者95例。通过生化分析和免疫组织化学检测, 分析不同供体来源肝组织损伤及补体活化水平, 并比较分析不同供体肝移植术后的并发症及生存率。结果与活体供肝比较, 脑死亡供体血清谷丙转氨酶(ALT)和谷草转氨酶(AST)水平更高(ALT:21.0 U/L比33.5 U/L;AST:23.0 U/L比36.0 U/L;P<0.01), 肝组织损伤苏木精-伊红(HE)染色评分更高(0.42比1.12, P<0.05)。移植后, 脑死亡供肝和活体供肝都受到损伤, 但脑死亡供体的肝损伤明显更严重, 术后血清转氨酶水平更高, 证实在人体肝移植中脑死亡同样存在诱导供肝移植术后级联损伤效应。相对于活体供者, 脑死亡供者血清ALT和AST水平波动更大。与活体供肝的受者比较, 脑死亡供肝移植术后急性排斥反应、急性肝衰竭和肺部感染等并发症显著升高(P<0.05)。对移植术...     

大鼠原位肝移植术后急性排斥反应中 Fractalkine的表达及意义

目的利用直视下套入式吻合肝动脉加袖套法吻合门静脉建立的大鼠全血供肝移植模型,研究同种异体大鼠肝移植术后早期急性排斥反应中Fractalkine（Fkn）的表达情况。方法制备SD-Wistar大鼠全血供肝移植模型,随机分为两组,每组20只。对照组：于移植术后第1天开始腹腔内注射生理盐水（3ml/kg）;实验组：于移植术后第1天开始腹腔内注射环孢素A（3mg/kg）。术后观察大鼠一般情况,并于第3、5及7天分别处死5只大鼠,取肝脏标本,观察移植肝组织排斥反应强度（rejection activity index,RAI）及Fkn表达情况;余大鼠观察生存时间。结果对照组存活18只,实验组存活19只。实验组较对照组术后一般情况好,存活时间为19.50±4.51d,与对照组7.60±1.60d比较,差异有统计学意义（P〈0.05）。组织学观察：对照组移植肝小叶结构清楚,汇管区增大,大量淋巴细胞浸润;实验组移植肝组织RAI明显降低。术后第3、5及7天,对照组RAI为3.80±0.35、5.90±0.87及7.50±1.30,实验组为3.10±0.21、3.90±0.41及4.50±0.52。两组术后第7天RAI比较差异有统计学意义（P〈0.01）。免疫组织化学观察：两组移植肝组织中均见细胞浆或细胞膜有棕色颗粒的Fkn表达,但实验组表达较弱。术后第3、5及7天,对照组Fkn细胞数为8.20±0.57、21.30±3.30及25.70±4.91,实验组分别为8.30±0.56、10.30±0.67及11.70±1.23;两组第5、7天比较差异有统计学意义（P〈0.01）。结论Fkn参与了同种异体大鼠肝移植急性排斥反应,可作为诊断大鼠肝移植急性排斥反应发生的指标之一。环孢素A可以通过抑制Fkn表达来抑制排斥反应发生的强度。     

Cytotoxic T-cell elimination during anti-CD4-induced rat liver acceptance and rapid replacement of functional graft antigen-presenting cells.

In previous studies, we showed that primed T cells were eliminated in long-term survival Wistar Furth (WF) recipient rats with spontaneously accepted Lewis (LEW) liver graft and that the grafted liver lost the ability to elicit rejection reaction early after liver transplantation. We hypothesized that the same phenomenon may be observed in tolerant animals after immunosuppression in a rejector rat strain combination (WF-->LEW). Furthermore, we proposed the repopulation of liver allograft with host antigen-presenting cells rapidly after transplantation. Recipient LEW rats that underwent anti-CD4 therapy accepted the WF liver allografts after a transient rejection reaction. In tolerant animals, alloreactive CD8 T cell precursors were present, but primed T cells were absent. Intraperitoneal challenge with grafted WF liver homogenates obtained from recipient LEW rats on day 4 after transplantation did not induce transient rejection responses in long-term survival recipient LEW rats, a finding that differed from the results of experiments using normal WF liver homogenates. However, challenge with grafted WF liver homogenates, similar to those of normal LEW liver homogenates, induced rejection responses in long-term survival recipient WF rats with LEW liver allograft. Flow cytometric analysis confirmed that most of nonparenchymal cells in the grafted WF liver were recipient (LEW) genotype. These observations showed that the deletional mechanism of effector T cells also is observed in this setting, and professional donor antigen-presenting cells are replaced by those of recipient genotype within the graft during the early phase of transplantation.     

Anti-CD4 induced rat heart tolerance: no presence of primed T cells and regulatory mechanisms for cytotoxic T cells

Treatment with anti-CD4 monoclonal antibody (mAb) (OX38) induces heart, but not skin graft tolerance in WF (RT1u) to Lewis (RT1l) rat strain combinations. We examined differences in cellular responses between heart-bearing and skin-rejected hosts that were both treated with anti-CD4 mAb. In the tolerant LEW rats bearing WF heart transplants, the secondary WF heart but not skin grafts were accepted. On the other hand, in anti-CD4 treated WF skin-rejected hosts, both secondary WF heart and skin grafts were rapidly rejected. Spleen cells from anti-CD4 treated WF skin-rejected LEW rats but not from WF heart-bearing LEW rats received the same treatment generated CTL after in vitro stimulation with paraformaldehyde (PFA) treated donor WF stimulator spleen cells. Adoptive transfer of spleen cells from WF skin-rejected LEW rats with or without anti-CD4 therapy into the tolerant LEW rats at the secondary WF heart transplantation blocked the secondary heart graft acceptance. However, transfer of spleen cells from WF heart-rejected rats without immunosuppression failed to block acceptance of the secondary heart graft. Our results indicated the lack of primed T cells and presence of regulatory mechanisms for tissue specific T cells in anti-CD4 treated heart bearing hosts.     

Influence of donor MHC class I antigen expression on graft survival after rat parathyroid allotransplantation

BACKGROUND AND AIMS: We investigated the influence of donor MHC antigen expression on graft survival after parathyroid transplantation in three different strain combinations. METHODS: MHC class I and II expression on parathyroid tissue of Lewis (LEW), Dark Agouti (DA), and Wistar-Furth (WF) rats was first analysed semiquantitatively by immunohistochemistry. Additionally, five groups were transplanted: (1) LEW to LEW, (2) DA to DA, (3) LEW to DA, (4) WF to LEW, and (5) DA to LEW. METHODS: MHC class I expression was strong in DA, moderate in WF, and weak in LEW rats; MHC class II expression was negative in all three strains. In the interstitium of all investigated tissue specimens, the proportion of MHC class II-expressing cells was low. RESULTS: After syngeneic transplantation, graft survival could be documented over the whole observation period. A mean graft survival of 20 (+/-2) days was observed following transplantation from LEW to DA, grafts in the group WF to LEW were rejected after 13 (+/-1) days, and graft function lasted 8 (+/-2) days in the group DA to LEW. The number of intragraft leukocytes expressing MHC class II molecules was equal in all groups, whereas increased levels of MHC class I on rat parathyroid tissue before transplantation resulted in a more rapid rejection. CONCLUSION: These results demonstrate that immunogenicity of rat parathyroid tissue seems to be determined by the amount of MHC class I expressed on donor parenchymal cells.     

Long-term survival of cardiac allografts in lethally irradiated rats repopulated with host-type hemopoietic cells.

To test the hypothesis that hemopoietic cells within a tissue graft are responsible for its immunogenicity, two experimental protocols were followed. LEW hearts were grafted into (LEW X BN)F-1 host rats and LEW or F-1 lymphocytes were injected into the apex of the grafted heart. The LEW but not the F-1 cells induced a local reaction, apparently because the circulating F-1 cells were the necessary immunogens. The second protocol took advantage of the knowledge that lethally irradiated LEW rats were able to reject WF Ag-B-incompatible hemopoietic cells (but not tissue allografts) within a few days. LEW rats were lethally irradiated and grafted with WF hearts on day 0. A mixture of LEW marrow, thymus, spleen and lymph node cells, or marrow cells only were infused either on day 0 or day 2. Cardiac allografts in hosts repopulated with the mixture of lymphoid cells survived a mean of 11.3 days in hosts infused on day 0, but survived indefinitely if the lymphoid cells were infused on day 2. The 2-day interval also prolonged the survival of allografts in rats infused with only marrow cells. The long-term recipients, without any further treatment, rejected WF skin grafts as first-set reactions 1 year later but did not reject second WF cardiac allografts. Lymphoid cells from long-term recipients imparied the rejection of WF cardiac allografts by LEW host rats. The lack of rejection of the original cardiac allograft supported the hypothesis tested. Certain hemopoietic cells responsible for the immunogenicity of cardiac allografts were probably eliminated in the 2-day interval at least in part by host effector cells capable of rejecting allogeneic hemopoietic cells. However, the mechanism of long-term "unresponsiveness" to WF hearts could have been caused by loss of accessory cells during the 2-day interval followed by infusion of immunocompetent cells. Skin rejections in these recipients may have been attributable to reactions against skin differentiation-specific antigens.     

Rat parathyroid allotransplantation: Influence of MHC antigen expression on graft survival

MHC antigen expression in parathyroid tissue and its influence on graft survival after allogeneic transplantation were investigated using a heterotopic rat transplantation model. MHC class I and II expression in parathyroid tissue of Lewis (LEW), Dark Agouti (DA), and Wistar-Furth (WF) rats was analysed semi-quantitatively by using immunohistochemistry. MHC class I expression was strong in DA, moderate in WF, and weak in LEW rats parenchyma, whereas MHC class II expression was negative. In the interstitium of all investigated tissue specimens, the proportion of MHC class II-expressing cells was low. Additionally, four groups were transplanted: 1) LEW to LEW, 2) DA to DA, 3) LEW to DA, and 4) WF to LEW. After syngeneic transplantation, graft survival could be documented over the whole observation period. A median graft survival of 20 (+/-2) days was observed after transplantation from LEW to DA, whereas grafts in the group WF to LEW were rejected after 13 (+/-1) days. The number of intra-graft leucocytes expressing MHC class II molecules was the same in all groups, whereas increased levels of MHC class I in parathyroid tissue before transplantation resulted in a more rapid rejection. These results indicate that immunogenicity of rat parathyroid tissue might be determined by the amount of MHC class I expressed in donor parenchymal cells. Further experiments are necessary to validate this observation.     

The effects of perioperative portal venous inoculation with donor lymphocytes on renal allograft survival in the rat. I. Specific prolongation of donor grafts and suppressor factor in the serum

In order to investigate the in vivo functional role of the liver in the immune responses in organ transplantation, effects of perioperative portal venous p.v. administration of donor lymphocytes on renal allograft survival were tested in the rat kidney transplant model. Donor lymphocytes were prepared from BN (BN, RT-1n) or third-party DA (RT1a) rat spleens and lymph nodes and injected p.v. or intravenously to Lewis (LEW, RT-1l) hosts on the day of transplantation (day 0). Untreated LEW hosts rejected BN renal grafts at 7.8 +/- 0.6 days (n = 10). Intravenous administration of 1 x 10(8) BN cells to LEW hosts on day 0 caused a slight, but not significant, prolongation of renal allograft survival (MST = 9.5 +/- 3.0 days, n = 13, NS), whereas portal venous inoculation of 1 x 10(8) BN cells on day 0 remarkably prolonged renal graft survival to 22.2 +/- 5.3 (n = 10, P less than 0.01). The prolongation of graft survival was antigen-specific; the administration of 1 x 10(8) DA cells p.v. to LEW hosts did not prolong the survival of BN renal grafts (MST = 7.4 +/- 0.8, n = 5). Spleen cells from p.v. treated LEW hosts 10 days after transplantation had no suppressor effect on the one-way MLC reaction of normal LEW responder cells toward donor BN or third-party DA stimulators. On the other hand, when serum from p.v.-treated LEW hosts was added to MLC at a concentration of 3 per cent of total volume, it suppressed the MLC reaction toward donor BN cells by 71.6 per cent, but not toward third-party DA stimulators (-8.5 per cent suppression, NS). Histological examination of p.v.-treated LEW hosts at 10 days after transplantation revealed that the liver had normal lobular architecture without expansion of portal tracts and infiltration of inflammatory cells. On the other hand, the transplanted kidney demonstrated a moderate mononuclear cell infiltration around the artery without an interstitial hemorrhage. Moreover, adoptive transfer of the serum from p.v.-treated LEW rats into the virgin secondary LEW hosts significantly prolonged the graft survival of BN kidneys from 7.8 days to 18.9 +/- 5.5 days (P less than 0.01), but not third-party DA graft survivals (MST = 7.5 +/- 0.6 days), indicating that an antigen-specific tolerogenic factor was released into the circulation through the process of allogeneic cells in the liver.     

Mobilization of host stem cells enables long-term liver transplant acceptance in a strongly rejecting rat strain combination

Careful examination of liver, kidney and heart transplants in human recipients has revealed small numbers of host bone marrow derived stem cells in the graft. If the limited recipient repopulation of a donor graft that is currently observed could be facilitated, it is possible that conversion to a predominantly host phenotype would permit long-term graft function without immunosuppression. We proposed to "engineer" repopulation after transplant in a strain combination (dark agouti [DA] to Lewis green fluorescent protein+[LEW GFP+]) which rejects liver grafts strongly, a model that more closely resembles the situation in humans. Treatment on days 0, 1, 2, 3 and 7 after transplantation with low-dose (0.1 mg/kg) tacrolimus (T) designed to blunt rejection combined with plerixafor (P) to mobilize host stem cells resulted in greater than 180 days graft survival with extensive albeit spotty conversion of a small (50%) DA graft to the recipient LEW GFP+ genotype. Subsequent skin grafting revealed donor-specific graft prolongation. The T plus P treatment resulted in higher levels of Lin-Thy1+CD34+CD133+ stem cells and Foxp3+ regulatory T cells in the blood and liver at day 7. Thus, pharmacological mobilization of host stem cells sustains liver allografts by two mechanisms: repopulation of injured donor cells and regulation of the immune response.     

Different kinetics of donor cell populations after isolated liver and combined liver/small bowel transplantation

Abstract Spontaneous tolerance induction after liver transplantation also supports additional transplants, e. g. a small bowel graft, from the same donor (tolerogenic effect). Chimerism serves as a possible explanation of this phenomenon. Isolated liver (LTx) and combined liver/small bowel transplantation (LSBTx) are compared. LSBTx and LTx were performed in the BN → LEW rat strain combination without immunosuppression. Parenchymal damage during rejection was monitored by sequential standard histology. Donor/recipient populations were identified and further differentiated for immunhistochemical single and double staining. A small number of donor specific leukocytes can be detected on all days in host organs (microchimerism). A significantly larger donor leukocyte population survives long‐term in the sinusoids of liver (graft chimerism). Sinusoidal donor leukocytes survive rejection and recover in number after tolerance induction. Rejection of liver allografts and infiltration by host leukocytes are more pronounced after LSBTx than after LTx. Accordingly, during rejection a steeper decline of sinusoidal donor leukocytes is observed after LSBTx and recovery after tolerance induction is not as marked. Microchimerism apparently plays no significant role in either transplantation model. The number of sinusoidal donor leukocytes, however, mirrors closely host immune responses.     

Successful living donor liver transplantation for severe hepatic GVHD histologically resembling autoimmune hepatitis after bone marrow transplantation from the same sibling donor

A 30‐year‐old woman developed severe liver dysfunction 1 year after bone marrow transplantation (BMT) from an HLA‐identical sibling donor for B lymphoblastic leukemia (B‐ALL) during the tapering of cyclosporin A. The histologic picture resembled autoimmune hepatitis (AIH), although neither autoantibody nor hypergammaglobulinemia was detected. She entered hepatic coma, and underwent living donor liver transplantation from the same donor on day 421 after BMT. She is well 18 months after the procedure, showing normal liver function and hematopoiesis. AIH‐like hepatic graft‐versus‐host disease (GVHD) has not been documented. This patient is the second case of living donor liver transplantation for hepatic GVHD from the same donor.