小鼠异基因造血干细胞移植后使用G-CSF对aGVHD的影响

 目的: 探讨小鼠异基因造血干细胞移植(allo-HSCT)后使用粒细胞集落刺激因子(G-CSF)对急性移植物抗宿主病(aGVHD)的影响及其可能的机制。方法: 以雄性C57BL/6小鼠(H-2^b)为异基因供鼠,雄性BALB/c小鼠(H-2^d)为同基因供鼠;以接受8 Gy[⁶⁰Co] γ射线全身照射(TBI)预处理雌性BALB/c小鼠为受鼠,并随机分为7组:单纯TBI组、同基因骨髓+脾细胞移植(Syn-BMST)组、异基因骨髓移植(allo-BMT)组、异基因骨髓+脾细胞移植(allo-BMST)组、Syn-BMST后G-CSF给药(Syn-BMST+G-CSF)组、allo-BMT后G-CSF给药(allo-BMT+G-CSF)组和allo-BMST后G-CSF给药(allo-BMST+G-CSF)组,各G-CSF给药组从移植后第1天(+1 d)开始皮下注射G-CSF 2 μg/d,观察至+60 d。比较各组生存时间、aGVHD发生情况和病理改变,流式细胞术检测骨髓H2-Kb⁺细胞百分率(异基因嵌合率),比较allo-BMST和allo-BMST+G-CSF组+10 d时血清细胞因子(IL-2、IL-4、IFN-γ和TNF-α)水平、脾总有核细胞数(SpTNC)和脾细胞免疫表型的差异。结果: 单纯TBI组小鼠于照射后9~15 d死于造血衰竭,其余各组+10 d时均100%获得造血重建,随机抽取2只异基因骨髓移植受鼠,+30 d供者细胞嵌合率分别为99.8%和99.4%,表明清髓性allo-HSCT模型建立成功。Syn-BMST、Syn-BMST+G-CSF、allo-BMT和allo-BMT+G-CSF组小鼠观察至+60 d均未发生aGVHD。与allo-BMST组相比,allo-BMST+G-CSF组受鼠出现aGVHD时间早、程度重、病理改变严重、存活时间明显缩短(P<0.05)、+10 d SpTNC明显增加(P<0.05)、脾脏NK细胞显著扩增 (P<0.01)、DC1/DC2比值减低(P<0.05),而2组血清IL-2、IL-4、IFN-γ和TNF-α水平差异无统计学意义。结论: 移植后使用G-CSF对小鼠异基因单纯骨髓移植后aGVHD无明显影响,但能显著加重allo-BMST后aGVHD的严重程度并缩短受鼠生存时间,该效应可能与G-CSF诱导供鼠NK细胞扩增有关,提示临床allo-HSCT后早期使用G-CSF可能触发或加重aGVHD的风险。     

异基因造血干细胞移植后肺部并发症的发生和危险因素分析

目的探讨治疗恶性血液病异基因造血干细胞移植（allo—HSCT）后肺部并发症与相关危险因素的关系。方法回顾性分析1991年8月至2004年6月157例allo—HSCT患者的临床资料。结果71例患者发生87例次肺部并发症，其中15例患者发生2次以上肺部并发症，总发生率为45.2％。直接死于肺部并发症者37例（23．6％），发生中位时间103d（1～886d）。其中细菌性肺炎32例，间质性肺炎8例，肺真菌病3例，肺水肿3例，肺结核2例，肺栓塞1例，2种或2种以上病原所致的肺部并发症38例次。单因素分析显示：患者年龄、疾病状态、供受者关系、HLA配型相合程度及广泛型慢性移植物抗宿主病（cGVHD）是影响移植后肺部并发症的危险因素。多因素分析显示：疾病状态和广泛型cGVHD与肺部并发症的发生显著相关（P＜0．01）。结论肺部并发症是allo—HSCT后常见的并发症之一。患者移植时疾病状态和广泛型cGVHD是与allo—HSCT后肺部并发症发生相关的危险因素。     

异基因造血干细胞移植后的相关并发症及危险因素

背景：有效预防和治疗异基因造血干细胞移植后并发症是提高患者存活率的重要因素。 目的：分析异基因造血干细胞移植后相关并发症的发生和危险因素。 方法：应用文献检索的方法获取异基因造血干细胞移植后相关并发症研究的文献,对符合研究标准的文献进行深入的数据分析,文章选取异基因造血干细胞移植后极易发生的并发症进行分析,如肺部并发症、真菌性败血症、巨细胞病毒感染以及中枢神经系统并发症等。 结果与结论：异基因造血干细胞移植后易出现肺部并发症,而且死亡率较高,肺部并发症的发病机制可能与移植物抗宿主病和巨细胞病毒抗原血症相关。异基因造血干细胞移植后真菌性败血症病原菌以假丝酵母菌属为主,死亡率较高,应二级预防性和早期经验性抗真菌治疗。更昔洛韦、膦甲酸钠对异基因造血干细胞移植后巨细胞病毒感染的治疗有效。中枢神经系统并发症在异基因造血干细胞移植后发生率较低,但在治疗过程也不容忽视。异基因造血干细胞移植后相关并发症的发生与多种危险因素有关,在临床治疗过程中要对相关因素采取预防措施,减少并发症的发生,提高患者的存活率。     

Renal thrombotic microangiopathy associated with chronic graft-versus-host disease after allogeneic hematopoietic stem cell transplantation

Thrombotic microangiopathy (TMA) is a major complication after hematopoietic stem cell transplantation (HSCT). In this study, we examined the clinical and pathologic features of 2 patients and 5 autopsy cases with HSCT-associated renal TMA to clarify the association between graft-versus-host disease (GVHD) and renal TMA. The median interval between HSCT and renal biopsy or autopsy was 7 months (range 3-42 months). Clinically, acute and chronic GVHD occurred in 7 and 4 patients, respectively. Clinical evidence for TMA was detected in 2 patients, while chronic kidney disease developed in all patients. The main histopathological findings were diffuse endothelial injury in glomeruli, peritubular capillaries (PTCs), and small arteries. In addition, all cases showed glomerulitis, renal tubulitis, and peritubular capillaritis with infiltration of CD3+ T cells and TIA-1+ cytotoxic cells, suggesting that GVHD occurred during the development of TMA. Diffuse and patchy C4d deposition was noted in glomerular capillaries and PTCs, respectively, in 2 biopsy and 2 autopsy cases, suggesting the involvement of antibody-mediated renal endothelial injury in more than 50% of renal TMA cases. In conclusion, the kidney is a potential target of chronic GVHD that may induce the development of HSCT-associated TMA. Importantly, some cases are associated with chronic humoral GVHD.     

Host MyD88 signaling protects against acute graft-versus-host disease after allogeneic bone marrow transplantation

Recent experimental strategies to reduce graft-versus-host disease (GVHD) have focused largely on modifying innate immunity. Toll-like receptor (TLR)-driven myeloid differentiation primary response 88 (MyD88)-dependent signalling pathways that initiate adaptive immune function are also critical for the pathogenesis of GVHD. This study aimed to delineate the role of host MyD88 in the development of acute GVHD following fully major histocompatibility complex-mismatched allogeneic bone marrow transplantation (BMT). When myeloablated BALB/c MyD88 knock-out recipients were transplanted with C57BL/6 (B6) donor cells, they developed significantly more severe GVHD than wild-type (WT) BALB/c hosts. The increased morbidity and mortality in MyD88^–/– mice correlated with increased serum levels of lipopolysaccharide and elevated inflammatory cytokines in GVHD target organs. Additionally, MyD88 deficiency in BMT recipients led to increased donor T cell expansion and more donor CD11c⁺ cell intestinal infiltration with apoptotic cells but reduced proliferation of intestinal epithelial cells compared with that in WT BMT recipients. Decreased expression of tight junction mRNA in epithelial cells of MyD88^–/– mice suggested that MyD88 contributes to intestinal integrity. Cox-2 expression in the GVHD-targeted organs of WT mice is increased upon GVHD induction, but this enhanced expression was obviously inhibited by MyD88 deficiency. The present findings demonstrate an unexpected role for host MyD88 in preventing GVHD after allogeneic BMT.     

Bone marrow-derived mesenchymal stem cells decrease acute graft-versus-host disease after allogeneic hematopoietic stem cells transplantation

Graft-versus-host disease is a major complication of allogeneic hematopoietic stem cells transplantation, leading to serious morbidity and mortality. Mesenchymal stem cells(MSC)from bone marrow cause immunoregulation in vitro and in vivo. They also have the potential to protect from lethal GVHD after both autologous and allogeneic Hematopoietic Stem Cells Transplantation (HSCT). In this study, we investigated the mechanisms responsible for GVHD in the allo-HSCT co-transplantation with MSC condition. The model of acute GVHD in Rats was established using allogeneic HSC with donor-derived T cells transplantation, with or without additional donor-derived MSC co-transplantation. The degrees of GVHD were compared, the differentiation of CD4⁺, CD8⁺, Th1/Th2 and CD4⁺CD25⁺ T cells in vivo were assessed by flow cytometry and RT-PCR analyses. We found that MSC inhibited lethal GVHD after allo-HSCT. The value of CD8⁺ and CD4⁺ T cells and the ratio of Th1/Th2 T cell subsets decreased, at the same time the proportion of CD4⁺CD25⁺ T cells increased both in spleen lymphocytes and thymocytes in vivo after allo-HSCT with MSC co-transplantation compared with conventional allo-HSCT. Our results strongly suggested that BM-derived MSC has the function of preventing lethal GVHD after allo-HSCT by means of homeostasis of T subsets in vivo.     

HLA单倍体相合与全相合外周血造血干细胞移植后的急性移植物抗宿主病

背景：异基因外周血造血干细胞移植成为造血干细胞移植的主要方式,近年来HLA单倍体相合造血干细胞移植因供者来源广泛在临床应用较多,急性移植物抗宿主病仍是影响移植成功率的主要因素。 目的：观察亲缘HLA单倍体相合与全相合异基因外周血造血干细胞移植后急性移植物抗宿主病的发生特点,探讨降低急性移植物抗宿主病发生率的方法及单倍体造血干细胞移植应用于临床的意义。 方法：行异基因外周血造血干细胞移植的患者52例,其中HLA全相合组31例,单倍体组21例。HLA单倍体组采用改良马利兰/环磷酰胺+兔抗人胸腺T细胞免疫球蛋白预处理方案,HLA全相合组采用改良马利兰/环磷酰胺预处理方案。移植物抗宿主病的预防采用短程甲氨蝶呤+环孢素A+吗替麦考酚酯的方案。 结果与结论：52例患者均获得完全持久干细胞植入。其中,急性移植物抗宿主病发病率为48%(25/52),Ⅲ-Ⅳ度急性移植物抗宿主病发病率为23%(12/52);全相合组及单倍体组急性移植物抗宿主病累积发病率分别为39%(12/31)和62%(13/21)(P > 0.05);全相合组及单倍体组Ⅲ-Ⅳ度急性移植物抗宿主病累积发病率分别为10%(3/31)和43%(9/21)(P < 0.05);发生于移植后+30 d、+31 d-+60 d、+61 d-+100 d的急性移植物抗宿主病类型分布差异无显著性意义(P > 0.05);发生在移植后+30 d内的急性移植物抗宿主病发生率高于移植后   +31 d-+60 d和+61 d-+100 d;发生急性移植物抗宿主病组和无急性移植物抗宿主病组复发率、2年无病生存率差异无显著性意义(P > 0.05),全相合组与单倍体组相比复发率差异无显著性意义(P > 0.05),2年无病生存率前者高于后者(P < 0.05)。说明采用上述移植方案,单倍体组安全性与疗效接近全相合组;在缺乏HLA相合供者时,单倍体造血干细胞移植是治疗恶性血液病的重要方法。中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程全文链接：     

CD40L表达在异基因造血干细胞移植中GVHD发生的意义

目的：初步探讨在异基因造血干细胞移植（HSCT）中发生移植物抗宿主病（GVHD）患者DC40L表达的变化以及意义。方法：HSCT治疗重型β-地中海贫血（n=12）和遗传性溶血性贫血（n=1）成功植入的儿童患者，其中脐血移植（UCBT）8例，异基因外周血造血干细胞移植(allo-PBSCT)5例，在移植前、移植后发生GVHD时采用流式细胞仪检测和比较外周血中CD40L和CD40的表达。结果：3例UCBT无GVHD，其余均发生了Ⅰ-Ⅳ度急性GVHD。急性GVHD发生时CD4^ CD40L^ 和CD8^ CD40LT细胞表达明显升高，allo-PBSCT者更明显；慢性GVHD发生时患者的CD40L^ 、CD25^ 和CD69^ 在CD4^ 和CD8^ T细胞上的表达亦增加。CD19^ CD40^ B细胞的表达在UCBT和allo-PBSCT的3个月内则一直处于低于正常的水平。结论：CD40L高表达与GVHD的发生相关，提示CD40-CD40L共刺激途径在GVHD的发生中可能起着重要作用。     

异基因造血干细胞移植CD94分子在T细胞高表达的意义初探

目的检测CD94分子在T细胞表达的水平,同时探讨在异基因造血干细胞移植(HSCT)中发生移植物抗宿主病(GVHD)患者CD94分子在T细胞表达的意义。方法HSCT治疗高危白血病和遗传性溶血性贫血成功植入的儿童患者,其中同胞脐血移植(UCBT)10例,非血缘相关UCBT1例,异基因外周血造血干细胞移植(alloPBSCT)5例,在移植前后发生GVHD时采用流式细胞仪检测和比较外周血中CD94的表达,并与正常外周血水平比较。结果CD94主要表达于CD3+CD8+T细胞,正常情况下外周血和脐血T细胞表达率低于10%,其中CD4+细胞几乎不表达,低于2%。但在UCBT或alloPBSCT后CD94在CD4+T细胞和CD8+T细胞均明显增高。3例UCBT无GVHD,其余均发生了ⅠⅣ0急性GVHD。急性GVHD发生时CD4+CD94+和CD8+CD94+T细胞表达明显升高。结论异基因造血干细胞移植后发生GVHD时,T细胞高表达CD94,可能是在同种抗原的刺激下机体自我保护的结果。     

单倍型异基因造血干细胞移植后发生巨细胞病毒感染的临床分析

目的 探讨单倍型异基因造血干细胞移植后发生巨细胞病毒(CMV)感染的临床特点及治疗.方法 对北京军区总医院血液科2011年1月-2013年1月采用单倍型异基因造血干细胞移植治疗的50例患者的临床资料进行回顾性研究,供者接受粒细胞集落刺激因子动员,采用骨髓加外周血干细胞联合移植,预处理方案以改良BUCY方案为主,移植后监测CMV-DNA,分析CMV感染的特点并探讨其治疗方法.结果 全部患者中男32例,女18例,年龄5-45岁,平均年龄23.8岁,其中共12例发生CMV血症,发生率为24％,首次检出CMV-DNA中位时间是移植后50天(36-72),CMV定量范围为2.4×103-6.2×106拷贝/mL,其中6例为CMV相关性出血性膀胱炎,2例为CMV相关性间质性肺炎,抗CMV治疗后全部患者CMV-DNA转阴.结论 单倍型异基因造血干细胞移植后巨细胞病毒感染发生率高,更昔洛韦、膦甲酸钠抗病毒治疗疗效可靠、不良反应少.     

Cytomegalovirus management after allogeneic hematopoietic stem cell transplantation: A mini-review

Because of the high incidence of cytomegalovirus (CMV) seropositivity in the population, CMV infection is a common and severe complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT) in Taiwan. Here we propose a CMV management strategy for patients undergoing allo-HSCT from the Taiwanese perspective, which focuses on the epidemiology, diagnosis, monitoring, prophylaxis, and treatment of CMV infection after allo-HSCT. In terms of CMV monitoring, weekly CMV monitoring with the COBAS® AmpliPrep system is the standard approach because the pp65 CMV antigenemia assay has a lower sensitivity than CMV monitoring with the COBAS® AmpliPrep system. However, pp65 CMV antigenemia assay has a better correlation with clinical symptoms in immunocompromised patients. A 14-week prophylactic course of letermovir is recommended for allo-HSCT recipients in Taiwan, especially for recipients of hematopoietic stem cells from mismatched unrelated and haploidentical donors. Preemptive ganciclovir therapy should be initiated when the CMV viral load exceeds 1000 copies/mL, and should not be discontinued until CMV DNA is no longer detected in the blood. For allo-HSCT recipients who have CMV-related diseases, ganciclovir with or without CMV-specific intravenous immunoglobulin is the standard of care. The limited availability of foscarnet, an alternative for patients who are not responsive to or cannot tolerate ganciclovir, is a crucial issue in Taiwan. For pediatric allo-HSCT recipients, more data are needed to propose a CMV management recommendation.     

造血干细胞移植治疗自身免疫性疾病

自从1995年造血干细胞移植（HSCT）应用于难治复发性自身免疫性疾病（AID）的治疗以来,取得了令人鼓舞的疗效,最近已经进入Ⅲ期临床试验阶段。AID可能是一种造血干细胞异常所致疾病,本文主要就自体或异体HSCT治疗AID的原理及自体HSCT治疗几种主要AID的临床试验结果做一综述。     

Differential diagnosis of skin lesions after allogeneic haematopoietic stem cell transplantation

Allogeneic haematopoietic stem cell transplantation (i.e. bone marrow or peripheral blood stem cell transplantation) is a common procedure in the treatment of various haematological disorders such as aplastic anaemia, (pre)leukaemias, some malignant lymphomas, multiple myeloma and immunodeficiency states. Many of these patients develop erythematous skin lesions following transplantation. Although graft- versus-host disease is the major differential diagnosis in these situations, many other causes of erythema are encountered. The large number of transplant patients means that more and more pathologists are confronted with the challenging problem of making a correct diagnosis in these situations. In this review article we therefore describe the different causes of erythema and their differential diagnoses. In most cases the clinical presentation is related to the microscopical features. Besides acute and chronic graft-versus-host disease, we discuss the (common) drug reactions and non-specific features such as Sweet's syndrome, erythema nodosum and eosinophilic folliculitis. In addition, we deal with the recurrence of original diseases and infections. With this knowledge every pathologist should feel comfortable when looking at skin biopsies of patients after haematological stem cell transplantation.     

骨髓间质干细胞降低大鼠移植物抗宿主反应的实验研究

目的 探讨MSCs对GVHD的作用及其机制.方法 建立大鼠同种异体骨髓移植模型,同时输入供者的T淋巴细胞诱导出移植物抗宿主反应,联合或不联合移植供体来源的MSCs,观察受鼠的生存时间,同时利用RT-PCR法研究Th1/Th2淋巴细胞亚群的比例,用ELISA法检测移植后体内IL-4细胞因子的浓度.结果 GVHD组的平均生存时间为(17.30±2.33)天,实验组的平均生存时间为(24.10±2.36)天 , 与单独移植HSCs相比,MSCs与HSCs共移植明显延长的受鼠的生存时间.同时,GVHD组Th1/Th 2 细胞比值为1.29±0.06,IL-4因子的浓度平均为(14.84±2.59) pg/mL,实验组Th1/Th 2细胞比值为(0.77±0.14),IL-4因子的浓度平均为(40.09±13.99) pg/mL.MSCs与 HSCs 共移植降低了体内Th1/Th2淋巴细胞亚群的比例,提高了体内IL-4细胞因子的浓度.结论 MSCs与HSCs共移植能有效抑制HSCs移植后致死性GVHD的发生,延长生存时间,同时MSCs 可能通过作用于体内Th1/Th2淋巴细胞亚群的比例,促进体内IL-4细胞因子的分泌从而间接发挥了抑制GVHD的作用.     

非清髓异基因造血干细胞移植治疗低增生性MDS1例并文献复习

目的探讨非清髓性异基因外周血造血干细胞移植治疗低增生性骨髓增生异常综合征（MDS）的疗效,观察其植入及并发症的发生情况。方法我院诊断为低增生性MDS患者1例,采用氟达拉滨＋阿糖胞苷＋环磷酰胺的非清髓预处理方案,环孢素A＋甲氨蝶呤＋骁悉预防移植物抗宿主病。结果 STR-PCR证实移植后30d及3个月骨髓植入为完全供者型,移植后3个月发生多发性脑梗塞,6个月出现面部皮疹及口腔溃疡,通过调整免疫抑制剂及输注间充质干细胞（5×10^7/次,2次）后症状明显好转。结论非清髓性异基因外周血造血干细胞移植治疗低增生性MDS获得较好的疗效。     

异基因造血干细胞移植治疗两例粘多糖累积症患儿

目的 探索造血干细胞移植治疗粘多糖累积症(mucopolysaccharidosis,MPS)的效果.方法 两例MPS患儿分别为MPS-Ⅰ H型和MPS-Ⅵ型,移植时年龄为23个月和18个月,均采用白舒菲20 ms/kg+环磷酰胺200 ms/ks进行预处理,干细胞分别来自9/10相合的无关供体和全相合同胞供体.结果 移植后11 d中性粒细胞达到0.5×109/L,14 d短串联重复序列.聚合酶链反应证实100%血细胞来自供体,移植后3个月疾病相关的酶活性分别达到70 mnol/h·mg和66 nmol/h·mg,移植后2年酶活性仍然维持在50.9nmoL/h·mg和44.5 nmol/h·mg.MPS-Ⅵ型患儿移植过程相当顺利,目前已随访28个月,健康状况良好.尽管MPS-Ⅰ H患儿移植中曾两次因肺炎合并急性心功能衰竭,但经紧急气管插管、机械通气等综合治疗后好转,随访至今也已25个月,目前心肺功能明显改善,肝脏缩小至正常大小,角膜混浊明显减轻,手指僵硬也有所改善.结论 异基因造血干细胞移植可用于治疗MPS-Ⅰ、MPS-Ⅵ;尽早移植可望减少移植相关并发症;移植所产生的临床效果需要更长时间的随访.     

Key factors in experimental mouse hematopoietic stem cell transplantation

The first mouse model of hematopoietic stem cell transplantation (HSCT) was developed more than 50 years ago. HSCT is currently being widely used in a broad range of research areas, which include studies of the engraftment process, the pathogenesis of graft-versus-host disease and possible ways of its treatment and prophylaxis, attempts to use the graft-versus-leukemia/tumor effect in treating hematological and oncological malignancies, cancer vaccine development, induction of transplanted organ tolerance, and gene therapy. However, although this model is widely distributed, many laboratories use different protocols for the procedure. There are a number of papers discussing different HSCT protocols in clinical work, but no articles summarizing mouse laboratory models are available. This review attempts to bring together different details about HSCT in the mouse model, such as the types of transplantation, possible pretreatment regimens and their combinations, methods and sources of graft harvesting and preparation for the transplantation procedure, the influence of graft cell dose and content on the engraftment process, the transplantation method itself, possible complications, symptoms and techniques of their prophylaxis or treatment, as well as follow-up and engraftment assessment. We have also tried to reflect current knowledge of the biology of the engraftment.     

Strategies to accelerate immune recovery after allogeneic hematopoietic stem cell transplantation

The interplay existing between immune reconstitution and patient outcome has been extensively demonstrated in allogeneic hematopoietic stem cell transplantation. One of the leading causes of infection-related mortality is the slow recovery of T-cell immunity due to the conditioning regimen and/or age-related thymus damage, poor naïve T-cell output, and restricted T-cell receptor (TCR) repertoires. With the aim of improving posttransplantation immune reconstitution, several immunotherapy approaches have been explored. Donor leukocyte infusions are widely used to accelerate immune recovery, but they carry the risk of provoking graft-versus-host disease. This review will focus on sophisticated strategies of thymus function-recovery, adoptive infusion of donor-derived, allodepleted T cells, T-cell lines/clones specific for life-threatening pathogens, regulatory T cells, and of T cells transduced with suicide genes.     

Occurrence,risk factors and outcome of adenovirus infection in adult recipients of allogeneic hematopoietic stem cell transplantation

BackgroundAdenovirus (ADV) infections can have a high mortality in immunocompromised patients and are difficult to treat.Objectives and study designWe retrospectively analyzed occurrence and risk factors of ADV infection in 399 adults with hematological disorders undergoing hematopoietic stem cell transplantation (allo-HSCT), focusing on alternative donor transplantation (ADT) and disseminated disease.ResultsADV infection occurred in 42 patients (10.5%). Disease was localized in 18 and disseminated in 6 patients. ADV infection was observed in 15% after ADT, performed in 29% of all recipients, and was less frequent (6%) in T-cell-replete (TCR) haploidentical transplantation using post-transplantation cyclophosphamide (PTCY) than in other ADT protocols. Lower age, the use of alternative donor grafts and acute graft-versus-host disease (GvHD) ≥ grade II were risk factors for ADV infection.After failure of standard antiviral treatment, three patients with disseminated ADV disease received one dose of ADV-specific T cells, resulting in virological response in 2/3 patients, clearance of ADV viremia in 2/2 patients, and survival of 1/3 patients; both patients with pneumonia died.ConclusionsADV infection was of moderate occurrence in our adult recipients of allo-HSCT despite a high proportion of potential high-risk patients receiving ADT. TCR strategies using PTCY might limit ADV complications in haploidentical transplantation. Despite feasible adoptive therapy strategies, outcome of disseminated disease remains dismal.