肿瘤抗原负载的树突状细胞对肝癌肿瘤浸润淋巴细胞体外抗瘤作用的影响

目的： 研究肿瘤抗原负载的树突状细胞（DCs）对原发性肝癌肿瘤浸润淋巴细胞(TILs)体外增殖和抗瘤作用的影响。 方法： 将自体肿瘤细胞匀浆粗提物(Tuly)与原发性肝癌患者外周血来源的DCs共培养以制备肿瘤抗原负载的DC(DCTuly)，将DCTuly与自体TILs在低浓度IL2(100 U/ml)中共培养，用FCM测定DCTuly 的表型以及与DCTuly混合培养前后的TILs表型，并计数TILs。用LDH法测定TILs的细胞毒作用。ELISA法检测TILs培养上清中IFNγ和TNFα的含量。 结果： DCTuly表面CD1a，CD83，CD80，CD86，CD40和HLA－DR分子表达水平增高（P<0.05）；DCTuly明显诱导TILs的增殖(P<0.01)及对自体肝癌细胞的细胞毒作用 (P<0.01), CD3+TILs增多（P<0.05）， CD4+TILs比例较混合前升高(P<001)，但仍以CD8+TILs为主。与DCTuly混合培养后第1,2天，TILs分泌IFNγ和TNFα的量明显提高(P<0.01)。 结论： 负载肿瘤抗原的DCs可促进TILs的增殖，增强TILs的特异性抗肿瘤活性。     

细胞因子诱导的杀伤细胞对宫颈癌细胞的体内外杀伤效应

目的：探讨细胞因子诱导的杀伤细胞（cytokineinduced killer cells,CIKs）对宫颈癌CasKi和Hela细胞的体内外杀伤效应。方法：从宫颈癌患者的外周血分离单个核细胞,以改良方法（不加IFNγ,只加IL2 和antiCD3抗体）刺激扩增得到CIKs,用流式细胞仪分析CIKs表型。ELISA法检测CIKs培养上清中IFNγ、IL2 和TNFα的分泌水平。LDH释放法检测CIKs对CasKi和HeLa细胞的杀伤作用。建立荷CasKi或Hela细胞小鼠模型,以1×106或1×107个CIKs小鼠静脉注射治疗,每周1次,连续治疗3周,检测小鼠移植瘤的体积和重量。结果：在抗CD3抗体和IL2的刺激下,宫颈癌患者外周血单个核细胞被诱导培养成CIKs,其中CD3+CD56+细胞得到大量扩增。PHA激活后,CIKs产生大量的IFNγ和TNFα,而IL2的分泌量较少。被激活的CIKs可显著地杀伤宫颈癌CasKi细胞和HeLa细胞,最大杀伤率分别达（43.2±1.8）%和（46.2±15）%,且呈剂量依赖性。体内抗肿瘤实验结果显示,CIKs能显著抑制小鼠皮下宫颈癌移植瘤的生长（P<0.01）。结论：本实验的改良方法能有效制备CIKs,该CIKs在体内外对宫颈癌CasKi 和 Hela细胞有明显的杀伤效应。     

紫杉醇联合顺铂诱导的凋亡卵巢癌细胞的免疫原性

目的: 探讨紫杉醇联合顺铂诱导凋亡的卵巢癌细胞被DCs交叉提呈后能否促进免疫应答。方法：常规贴壁法刺激正常人外周血单核细胞分化诱导为DCs,6 d后将DCs和紫杉醇联合顺铂体外诱导的凋亡人卵巢癌细胞HO8910共同培养（凋亡组）,并以冻融细胞共培养DCs组(冻融组)或单独DCs组(空白组)作对照,以激光共聚焦扫描和流式细胞仪检测不同培养组DCs的分化和成熟程度。分别将各组成熟DCs与同一来源的磁珠分选的CD8+T细胞共培养, 3HTdR掺入法检测其增殖能力;LDH释放反应检测CTL对肿瘤细胞的杀伤能力;同时应用ELISPOT图像分析仪检测致敏后CD8+T细胞INFγ的分泌能力。结果：(1)紫杉醇联合顺铂诱导的凋亡卵巢癌细胞可被DCs有效吞噬,并促进DCs的成熟及其抗原提呈作用;(2) 3HTdR检测显示凋亡肿瘤细胞能诱导CD8+T细胞增殖（P<0.05）;(3)LDH释放实验与ELISPOT图像分析均证明凋亡肿瘤细胞诱导的CTL杀伤活性显著强于冻融组和空白组细胞（P<0.01）。结论：紫杉醇联合顺铂诱导的凋亡卵巢癌细胞具有较强的免疫原性,可促进DCs分化和成熟,进一步促进CD8+T细胞增殖、分泌与杀伤功能。     

CD40L+肺癌细胞抗原负载DC诱导同源肺癌免疫

目的：探讨CD40L+肺癌细胞抗原负载由人外周血单个核细胞（peripheral blood mononuclear cell,PBMC）诱导的DC对同源肺癌的免疫增强作用及其机制。方法：常规方法从正常成人外周血中分离PBMC、诱导分化成DC,以重组载体pDNA3.1-CD40L+转染A549肺癌细胞,制备已转染肺癌细胞抗原对DC进行负载刺激,通过流式细胞术检测DC的CD83、CD86及HLA-DR分子表达,ELISA法检测DC的IL-12分泌水平,再以MTT法检测DC对同源T淋巴细胞增殖状态以及A549肺癌细胞增殖影响,并与空载转染的A549细胞抗原诱导DC的相同功能进行对比。结果：将PBMC成功诱导分化出成熟的DC。重组CD40L诱导组DC的CD83、CD86及HLA-DR分子表达水平明显高于空载组\[(4.78±1.5）% vs （3.38±1.5）%、（9.79±5.27）% vs （5.53±2.17）%和 （11.84±8.31）% vs （537±5.48）%,均P<0.05\];IL-12分泌水平也高于空载组和未转染组（P<0.05)。CD40L+DC可促进T淋巴细胞的增殖(P<0.05),并导致同源T细胞对肺癌A549细胞增殖的抑制作用强于对照组、未转染组和空载组（P<0.05）。结论： CD40L转染肺癌细胞抗原诱导成熟的DC可以增强同源肺癌细胞的特异免疫能力。     

DC-CIK对急性髓细胞白血病干细胞的杀伤作用

目的:研究树突状细胞(dendritic cell,DC)联合同源细胞因子诱导的杀伤细胞(cytokine-induced killer cell,CIK)对急性髓细胞白血病细胞株KG-1a中白血病干细胞(leukemic stem cell,LSC)的体外杀伤和诱导凋亡作用。方法:分离健康人外周血单个核细胞,贴壁细胞用GM-CSF和IL-4诱导培养DC,悬浮细胞用IL-2、IL-1、IFN-γ和CD3 mAb诱导培养CIK。将KG-1a细胞冻融物作为抗原负载DC(即Ag-DC),与CIK共培养作为实验组(Ag-DC-CIK),无抗原负载的DC与CIK共培养作为对照组(DC-CIK),单独CIK作为空白对照组,与KG-1a共育后流式细胞术检测各组细胞中CD34+CD38-CD123+白血病干细胞的比例。DC-CIK与KG-1a细胞共培养,流式细胞术检测各组细胞中KG-1a细胞与CD34+CD38-CD123+细胞的凋亡率。结果:外周血单个核细胞成功诱导DC。CIK组、DC-CIK组及Ag-DC-CIK组中CD3+CD56+细胞比例为(17.36±4.44)%、(28.22±3.66)%和(36.16±5.88)%,依次升高(P<0.05)。与对照组相比,Ag-DC-CIK组与DC-CIK组细胞中CD34+CD38-CD123+细胞比例显著降低[(8.78±0.62)%vs(3.95±0.53)%、(3.03±0.62)%,P<0.01〗。DC-CIK可诱导KG-1a细胞凋亡,凋亡率由(2.34±0.74)%上升至(12.27±1.01)%,但对其中CD34+CD38-CD123+细胞无明显的诱导凋亡作用。结论:DC联合CIK能杀伤急性髓细胞白血病干细胞,但无明显的诱导凋亡作用。     

修饰的肿瘤抗原肽CEA-610D疫苗的体外抗肿瘤作用

目的: 评价修饰的CEA610D抗原肽疫苗体外抗肿瘤免疫的有效性,为其临床应用提供依据。方法： 多肽固相合成法合成HLAA2 CEA修饰肽(CEA610D)、HLAA2天然肽CEA605613（天然肽）和HLAA2无关肽MAGE3（无关肽）,采用同种异体混合淋巴细胞与肽共孵育的方法,诱导肽特异性细胞毒性T淋巴细胞(CTL),利用MTT法检测CTL的增殖和杀伤活性;流式细胞术观察细胞表型;RTPCR检测细胞穿孔素的表达;ELISA法检测CTL上清中IFNγ的水平。结果：CEA610D疫苗产生肽特异性CTL的能力最强（P<0.05）,其CD8+T细胞数也高于天然肽组和无关肽组;在效靶比为40〖DK〗∶1时,CEA610D和天然肽所诱导的CTL对CEA+HLAA2限制性人结肠癌细胞T84的杀伤活性可达(56.7±3.73)%和(51.2±1.86)%,而3种肽特异性CTL细胞对CEA+HLAA2人结肠癌lovo细胞杀伤活性维持在本底水平;CEA610D组的CTL所释放的杀伤相关介质穿孔素和上清中IFNγ的水平也显著高于其余两组（P<0.01）。结论：与天然肽相比,CEA610D疫苗可打破自身表位的免疫耐受,在体外抗肿瘤免疫中更具优势。     

CIK细胞对裸鼠肝癌移植瘤生长的抑制作用

目的：观察外周血单个核细胞(PBMC)体外经IFNγ， rIL2和antiCD3McAb诱导后细胞表型的变化及CIK细胞对裸鼠肝癌移植瘤的抑制作用。方法：采用成份血采血机采集6例健康自愿者PBMC，经多因子诱导后，计数活细胞数，流式细胞仪检测细胞表型；裸鼠肩胛下接种肝癌细胞，次日起连续6 d给予不同数量的CIK细胞，观察对肝癌生长的抑制作用。结果：诱导培养后13 d，效应细胞增殖7.1倍，CD3+CD56+双阳性细胞增殖约6倍。动物实验结果表明，CIK细胞可明显抑制肝癌移植瘤的生长，且肿瘤抑制率与CIK细胞的数量呈剂量效应关系。结论：PBMC细胞体外经多因子诱导成CIK细胞，其数量及抗肿瘤活性显著增加，对肝癌细胞的生长具有明显的抑制作用。     

DC-CIK细胞治疗晚期结直肠癌的临床疗效

目的：评价自体树突状细胞 (dendritic cell, DC) 联合细胞因子诱导的杀伤(cytokine-induced killer, CIK) 细胞治疗晚期结直肠癌患者的临床疗效和安全性。方法： 采集2011年7月至2015年3月解放军第81医院肿瘤生物治疗科收治的142例Ⅲ~Ⅳ期结直肠癌患者的外周血单个核细胞 (peripheral blood mononuclear cell, PBMC),经实验室体外诱导培养DC和CIK细胞。DC细胞通过结肠癌细胞株COLO 320或直肠癌细胞株HCT-116裂解物致敏后与CIK细胞回输至结直肠癌患者,观察DC-CIK细胞治疗的临床疗效和安全性。结果： 142例晚期结直肠癌患者经DC-CIK细胞免疫治疗后,客观缓解率为162%,疾病控制率为60.6%;1年生存率为47%,2年生存率为31%,3年生存率为31%;经细胞治疗后外周血CD3+T细胞、CD4+T细胞、CD8+T细胞、CD3+CD56+ NK细胞、CD4+CD25+ Treg细胞比例、CD4+/CD8+比值及癌胚抗原(carcinoembryonic antigen, CEA) 水平均无显著变化;单因素分析显示,TNM分期 (P=0.015)、治疗次数 (P=0.037) 及治疗前CEA值的正常与否为DC-CIK治疗结直肠癌的预后影响因素;多因素分析显示,治疗次数 (P=0.024) 和年龄 (P=0.015) 与DC-CIK治疗结直肠癌的预后密切相关。结论： DC-CIK细胞免疫治疗可能改善晚期结直肠癌患者远期生存率,可产生临床获益,无明显不良反应,安全可行。     

CD4+CD25+CCR6+调节性T细胞在小鼠乳腺癌模型中对CD8+T细胞的抑制作用

目的：观察CD4+CD25+CCR6+调节性T细胞（简称CCR6+Tregs）体内对CD8+T细胞功能的抑制作用,并探讨其与肿瘤免疫逃逸的关系。方法：建立4T1乳腺癌细胞荷瘤裸鼠模型,FACS分选CCR6+Tregs,检测其Foxp3的表达;FACS分选4T1特异性CD8+T细胞,CFSE标记后分别与CCR6+Tregs或CCR6Tregs共同过继转输入4T1荷瘤裸鼠体内,观察荷瘤裸鼠肿瘤生长情况和小鼠存活时间;FACS检测肿瘤组织中CD8+T细胞的增殖、细胞因子IFNγ的产生和颗粒酶B的表达情况。结果：CCR6+Tregs和CCR6Tregs均高表达Foxp3;CCR6+Tregs和CD8+T细胞共转输组4T1荷瘤裸鼠肿瘤的生长明显快于CCR6Tregs共转输组和CD8+T细胞单转输组,同时该组荷瘤裸鼠生存时间也明显缩短（P<0.05）;CCR6+Tregs和CD8+T细胞共转输组CD8+T细胞的增殖、IFNγ的产生和颗粒酶B的表达均明显低于CCR6Tregs共转输组和CD8+T细胞单转输组（P<0.05）。结论：CCR6+Tregs在体内可以有效抑制CD8+T细胞的功能,其在肿瘤免疫逃逸和肿瘤发生、发展中发挥重要作用。     

DC-CIK细胞免疫治疗胃癌的临床疗效及预后分析

目的：回顾性分析自体DC联合CIK（DC-CIK）细胞治疗96例胃癌患者的临床疗效和安全性。方法：采集2011年8月至2016年4月解放军第86医院肿瘤科及解放军第81医院肿瘤生物治疗中心收治的96例胃癌患者的外周血单核细胞 (peripheral blood mononuclear cell, PBMC),经实验室体外诱导培养DC和CIK细胞,DC通过胃癌MGC-803细胞裂解物致敏后与CIK细胞回输给患者,观察DC-CIK细胞治疗胃癌患者的临床疗效和安全性。结果：96例胃癌患者经DC-CIK细胞免疫治疗后,客观反应率为15.6%,疾病控制率为55.2%;1年生存率为56.0%,36~56个月总生存率维持在37.0%。免疫细胞治疗前后患者外周血肿瘤标志物CEA、CA199和CA724值均无明显变化。细胞治疗后患者外周血CD4+CD25+细胞比例显著下降\[（3.22±1.20)% vs (2.46±1.04)%,P<0.01\],CD3+、CD4+、CD8+、CD3+CD56+细胞百分比及CD4+/CD8+比值均无显著变化(P>0.05)。单因素分析显示,TNM分期、细胞治疗次数、治疗前CEA和CA199值为DC-CIK治疗胃癌预后的影响因素（P<0.05）;多因素分析显示,细胞治疗次数、治疗前CEA和CA199值与DC-CIK细胞治疗胃癌患者的预后相关（P<005）。结论：DC-CIK细胞免疫治疗对于胃癌患者是一种安全有效的治疗方式,多次治疗可能提高患者远期生存率。     

Low incidence of posttransplant lymphoproliferative disorder after allogeneic stem cell transplantation in patients with lymphoma treated with rituximab

Posttransplant lymphoproliferative disorder (PTLD) is a serious complication after hematopoietic stem cell transplantation (HSCT). Several studies of risk factors for PTLD have been reported; however, the probability of, and risk factors for, PTLD in patients with lymphoma is unknown. Japanese nationwide transplant registry data from 5270 patients with lymphoma after allogeneic HSCT were analyzed. Mature B-cell, T/NK-cell, and T-cell lymphoblastic subtypes accounted for 49%, 26%, and 9.6% of lymphoma cases, respectively. Rituximab was used in 1678 lymphoma patients, most of whom (89%) received HSCT for mature B-cell lymphoma. Thirty-one patients with lymphoma developed PTLD, representing a probability of 0.77% at 2 years post-HSCT, which did not differ significantly from that in patients with other diseases (P = .98). Year of HSCT after 2010 (hazard ratio [HR] = 5.6, 95% confidence interval [CI], 1.48-21.3), antithymocyte globulin (ATG) use in the conditioning regimen (HR = 4.5, 95% CI, 1.61-12.5), and no rituximab use before HSCT (HR = 3.2, 95% CI, 1.26-7.90) were identified as risk factors for PTLD. Probabilities of PTLD at 1 year post-HSCT according to rituximab and ATG use were 0.23% (rituximab+, ATG−), 0.75% (rituximab−, ATG−), 1.25% (rituximab+, ATG+), and 3.53% (rituximab−, ATG+). Regarding lymphoma subtypes, patients with mature B-cell lymphoma had the lowest incidence of PTLD (0.35% at 2 years). Among high-risk patients receiving ATG, the mortality rate due to infection was elevated in those previously treated with rituximab (22%) relative to those without (14%); however, the difference was not significant (P = .10). Rituximab use before HSCT significantly reduces the risk of PTLD. Adding rituximab to the conditioning regimen is potentially a good strategy to prevent the development of PTLD in high-risk patients.     

HeLa细胞HSP-70多肽体外诱导免疫活性细胞及其抗瘤机理

[目的]探讨用HeLa细胞HSP 70多肽诱导免疫活性细胞 (immunecompetentcells ,ICC)的特异性抗肿瘤机制。[方法]用热休克处理的HeLa细胞提取的HSP 70多肽剌激正常人外周血单个核细胞 ,在剌激扩增前后测定T淋巴细胞表型 ,并测定扩增的免疫活性细胞对HeLa细胞的杀瘤活性。[结果]在扩增的细胞中CD3+、CD8+淋巴细胞百分率明显增高 (P<0.01)。该免疫活性细胞对Hela细胞和来源于病人的宫颈癌细胞都具有较高的杀伤活性 ,而对经HSP 70单抗封闭后的HeLa细胞的杀伤率则明显下降。[结论]HeLa细胞HSP 70多肽能有效刺激PBMCs诱导活化免疫活性细胞 ,该免疫活性细胞具有特异性抗肿瘤作用     

Epstein–Barr virus-related lymphoproliferative disorder induced by equine anti-thymocyte globulin therapy

Post-transplant lymphoproliferative disorder (PTLD) is generally caused by an uncontrolled B-cell proliferation induced by Epstein-Barr virus (EBV) in the setting of impaired EBV-specific T-cell immunity. PTLD has been described in allogeneic hematopoietic stem cell transplant (HSCT) and rarely in autologous HSCT. Anti-thymocyte globulin (ATG) is being increasingly utilized for acute rejection in organ transplantation, severe autoimmune diseases and aplastic anemia. Mainly, the use of rabbit ATG has been associated with PTLD, which is considered to be more immunosuppressive than equine ATG. The sole administration of equine ATG has rarely been associated with PTLD. Due to the increased use of these potent and novel immunosuppressive agents, it is paramount to be aware of these complications. We present a 55-year-old man with an autologous HSCT who presented with an unusual case of monoclonal plasmacytic PTLD. His lymphoproliferative disorder occurred 3 years after his HSCT and 1 month after the use of equine ATG administered for severe aplastic anemia. We review current concepts of EBV-PTLD, including risk factors, the potential for preemptive therapy and various management strategies.     

Graft-versus-Tax response in adult T-cell leukemia patients after hematopoietic stem cell transplantation

Adult T-cell leukemia (ATL) caused by human T-cell leukemia virus type I (HTLV-I) is characterized by poor prognosis after chemotherapy. Recent clinical trials have indicated, however, that allogeneic but not autologous hematopoietic stem cell transplantation (HSCT) for ATL can yield better clinical outcomes. In the present study, we investigated cellular immune responses of ATL patients who obtained complete remission after nonmyeloablative allogeneic peripheral blood HSCT from HLA-identical sibling donors. In the culture of peripheral blood mononuclear cells (PBMCs) from a post-HSCT but not pre-HSCT ATL patient, CD8(+) CTLs proliferated vigorously in response to stimulation with autologous HTLV-I-infected T cells that had been established before HSCT in vitro. These CTLs contained a large number of monospecific CTL population directed to a HLA-A2-restricted HTLV-I Tax 11-19 epitope. The frequency of Tax 11-19-specific CD8+ CTLs in this patient markedly increased also in vivo after HSCT, as determined by staining with HLA-A2/Tax 11-19 tetramers. Similar clonal expansion of HTLV-I Tax-specific CTLs exclusively directed to a HLA-A24-restricted Tax 301-309 epitope was observed in the PBMCs from another ATL patient after HSCT from a HTLV-I-negative donor. Among four post-HSCT ATL patients tested, HTLV-I-specific CTLs were induced in the PBMC culture from three patients but not from the remaining one who had later recurrence of ATL. These observations suggested that reconstituted immunity against antigen presentation in ATL patients after HSCT resulted in strong and selective graft-versus-HTLV-I response, which might contribute to graft-versus-leukemia effects.     

Post‐transplant lymphoproliferative disease of donor origin,following haematopoietic stem cell transplantation in a patient with blastic plasmacytoid dendritic cell neoplasm

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an extremely rare condition that originates from dendritic cells. We report on the first case of Epstein–Barr virus (EBV)‐driven post‐transplant lymphoproliferative disorder (PTLD) of donor origin in a BPDC patient post‐allogeneic haematopoietic stem cell transplantation (HSCT). Flow cytometry study identified a cell population CD4+/CD56+/CD45RA+/CD123+/TCL1+ suggestive of BPDCN diagnosis, which was confirmed by a lymph node biopsy (cells positive for BCL11a, BDCA‐2, CD2AP, CD123, TCL1 and S100). Cytogenetic analysis revealed a complex karyotype: (19 metaphase) 47,XX,t(1;6)(q21;q2?5),‐13 + 2mar[11]/47, XX, +21 [3]/46,XX [5]. The patient was started on acute myeloid leukaemia (AML) induction schedule, and subsequently an allogeneic HSCT was performed. On day +36 post‐HSCT, bone marrow biopsy/aspirate showed complete morphological remission, and chimerism study showed 100% donor chimera. However, on day +37, the patient was found to have enlarged cervical and supraclavicular lymphoadenopathy, splenomegaly and raised lactic dehydrogenase. EBV‐DNA copies in blood were elevated, consistent with a lytic cycle. A lymph node biopsy showed EBV encoded RNA and large atypical B cells (CD45dim?, CD4+/CD56+, monoclonal for k‐chain, CD19+/CD20+/CD21+/CD22+/CD38+/CD43+/CD79β?/CD5?/CD10?), consistent with PTLD monomorphic type. Chimerism study showed that PTLD was of donor origin. This case together with the recent literature findings on BPDCN and PTLD are discussed. Copyright © 2012 John Wiley & Sons, Ltd.     

Primary central nervous system post-transplant lymphoproliferative disorders following allogeneic hematopoietic stem cell transplantation

Post-transplant lymphoproliferative disorder (PTLD) is a serious complication after allogeneic hematopoietic stem cell transplantation (HSCT). Extra nodal involvement is common in PTLD, but isolated involvement of the central nervous system (CNS) is extremely rare. Given the rarity of primary CNS-PTLD there is no consensus on optimal treatment. We report a patient who developed Epstein-Barr virus related primary CNS-PTLD following allogeneic HSCT who was treated with the monoclonal anti-CD20 antibody rituximab and reduction of immunosuppression. In addition, we review the literature and discuss treatment options for patients with primary CNS-PTLD following allogeneic HSCT.     

HeLa细胞HSP-70体外诱导抗瘤免疫活性细胞的研究

背景与目的:近来的研究证实,动物肿瘤细胞表达的热休克蛋白(heatshokproteinHSP)可携带肿瘤抗原,并能诱导抗瘤特异性T淋巴细胞的免疫应答。本文旨在探讨用HeLa细胞HSP-70多肽诱导的免疫活性细胞(immunecompetentcell,ICC)及其特异性抗肿瘤机制。方法:用热休克处理的HeLa细胞提取的HSP-70多肽剌激正常人外周血单个核细胞(PBMCs),在剌激扩增前后测定T淋巴细胞表型,并测定扩增的免疫活性细胞对HeLa细胞的杀瘤活性。结果:在扩增前后CD3+淋巴细胞百分率为(57.68±1.46)%和(85.73±1.44)%(P<0.002),CD8+淋巴细胞百分率为(23.56±1.86)%和(48.06±1.66)%(P<0.002)。该免疫活性细胞对HeLa细胞和来源于病人的宫颈癌细胞都具有较高的杀伤活性犤(82.69±1.97)%和(62.11±1.61)%犦,而对经HSP-70单抗封闭后的HeLa细胞的杀伤活性犤(31.05±2.09)%犦则明显下降。结论:HeLa细胞HSP-70多肽能有效刺激PBMCs诱导活化免疫活性细胞,该免疫活性细胞具有特异性抗肿瘤作用。     

Fulminant Epstein-Barr virus (EBV)-associated T-cell lymphoproliferative disorder with hemophagocytosis following autologous peripheral blood stem cell transplantation for relapsed angioimmunoblastic T-cell lymphoma

Post-transplant lymphoproliferative disorder (PTLD) is a complication that can develop after either solid-organ or hematopoietic stem cell transplantation (HSCT). T-cell PTLD is a rare disorder, especially following autologous HSCT. Here we report a case of T-cell PTLD which occurred after autologous peripheral blood stem cell transplantation (PBSCT) for relapsed angioimmunoblastic T-cell lymphoma (AILT). Three months after the transplant, the patient developed fever with elevated plasma Epstein-Barr virus (EBV)-PCR values. The patient subsequently developed pneumonitis, hepatomegaly and marked pancytopenia due to hemophagocytosis. The patient died of multi-organ failure, despite antiviral and steroid pulse therapy. Our post-mortem study confirmed the marked proliferation of EBV-infected T-cells that differed from the original AILT clone and macrophages/histiocytes were observed in the marrow, liver, lymph nodes and lungs. Phagocytosis was most evident in the bone marrow. The patient's AILT remained in complete remission. To the best of our knowledge, this is the first case of fulminant EBV-associated T-cell lymphoproliferative disorder (LPD) following autologous HSCT.     

Epstein-Barr virus-associated post-transplant lymphoproliferative disease with central nervous system involvement after unrelated allogeneic hematopoietic stem cell transplantation

Post-transplant lymphoproliferative disorders (PTLD) represent an heterogeneous group of abnormal lymphoid proliferation related to Epstein-Barr virus (EBV) reactivation that arise early after allogeneic hematopoietic stem cell transplant (HSCT). PLTD with central nervous system (CNS) involvement has been reported in few cases. We describe the case of a 31-year-old-man who developed an EBV-related PTLD with CNS involvement 2 months after an allogeneic unrelated HSCT for acute myeloid leukemia in first complete remission who was successfully treated with rituximab, cidofovir and intrathecal infusion of methotrexate and methylprednisolone.     

Hodgkin's disease as unusual presentation of post-transplant lymphoproliferative disorder after autologous hematopoietic cell transplantation for malignant glioma

Background  

Post-transplant lymphoproliferative disorder (PTLD) is a complication of solid organ and allogeneic hematopoietic stem cell transplantation (HSCT); following autologous HSCT only rare cases of PTLD have been reported.