ImmuKnow^TM免疫细胞功能检测在肝移植术后排斥反应中的意义

目的探讨CD4T淋巴细胞内ATP检测在肝移植术后排斥反应中的作用及意义。方法选取肝移植术后患者101例,共采集外周血样本142例次。标本检测采用ImmuKnow^TM免疫细胞检测试剂盒进行。根据患者是否发生排斥反应及不同的免疫状态,分析CD4^＋T淋巴细胞内ATP与肝移植术后排斥反应的关系。结果本组患者共发生排斥反应5例次,排斥反应组与非排斥反应组的CD4^＋T淋巴细胞ATP值分别为（762．00±135．34）、（390．23±238．77）ng／ml,P=0．001。低免疫应答组、正常免疫应答组和高免疫应答组肝移植术后排斥反应发生率分别为0、1．7％（1／59）和9．3％（4／43）,P=0．044。他克莫司（FK506）低浓度组和高浓度组CD4^＋T淋巴细胞ATP值比较无统计学差异,FK506浓度与CD4^＋T淋巴细胞ATP无直线相关关系（r=-0．055,P=0．518）。结论外周血CD^＋T淋巴细胞ATP对肝移植术后排斥反应的防治有重要意义。     

1型糖尿病患者外周血中CD4^＋CD25^＋与CD8^＋CD28^-调节性T细胞水平的研究

流式细胞仪检测1型糖尿病（T1DM）患者外周血CD4^＋CD25^＋与CD8^＋CD28^-调节性T细胞的水平,发现其外周血CD4^＋CD25^＋T淋巴细胞水平[（2．02±0．43）％]显著低于2型糖尿病（T2DM）组[（6．79±1．75）％]和健康对照（NC）组[（7．84±1．45）％],而CD8^＋CD28^-调节性T细胞水平三组间无差异。     

香烟烟雾提取物对CD4^＋T细胞向Th17细胞和调节性T细胞分化的影响

目的观察香烟烟雾提取物（CSE）对CD4^＋T细胞向Th17细胞和调节性T细胞分化的影响,为探索香烟烟雾暴露导致气道慢性炎症的机制提供实验依据。方法采用免疫磁珠法分离纯化健康志愿者外周血CD4^＋T细胞,以1×10^6／ml细胞密度接种于96孔培养板,分为以下8个组①空白对照组;②T细胞刺激剂组：加入T细胞刺激剂抗人CD3／28抗体微磁珠;③T细胞刺激剂CSE干预组：CD3／28＋2%CSE;④细胞因子组：CD3／28＋细胞因子;⑤细胞因子CSE干预组：CD3／28＋细胞因子＋2％CSE;⑥芳香烃受体（AHR）激动剂6-甲酰基吲哚[3,2-b]咔唑（FICZ）组CD3／28＋细胞因子＋FICZ;⑦AHR拮抗剂白藜芦醇组：CD3／28＋细胞因子＋2％CSE＋白藜芦醇;⑧溶剂对照组：CD3／28＋细胞因子＋DMSO。细胞因子为含TGF-β/IL-1β／IL-6／IL～23的混合细胞因子,以诱导Th17细胞和调节性T细胞分化。培养5d后,收集细胞,采用流式细胞术检测细胞表面分子CD4^＋CD25^＋Foxp3^＋细胞（Treg细胞）,以及胞内细胞因子IL-17＋的CD4^＋T细胞（Th17细胞）,计算各种刺激培养条件下,诱导生成的Th17及Treg细胞占CD4^＋T细胞的百分比。结果①CSE对Th17细胞分化的影响：空白对照组Th17细胞比例为（0．69±0．12）％,加入T细胞刺激剂后为（1．32±0．12）％,在此基础上加入CSE的干预组IL-17＋细胞比例升高为（2．17±0．24）％,（t=3．21,P〈0．01）;细胞因子组IL-17＋细胞比例为（1．35±0．08）％,而在此基础上加入CSE的干预组Th17细胞升高为（2．58±0．39）%（t=3．13,P〈0．01）。②CSE对Treg细胞分化的影响：在空白对照组中,Treg细胞占CD4^＋T细胞中的比例为（0．21±0．19）％,在加入T细胞刺激剂后,Treg细胞比例升高（3．59±0．37）％,加入细胞因子后,Treg细胞比例明显增加（5．85±0．76）％;在继续加入CSE干预后,Treg细胞比例明显减少（3．07±0．33）％（t=3．74,P〈0．01）;同样,T细胞刺激剂CSE干预组也出现Treg细胞比例减少（2．19±0．19）％,（t=2．71,P〈0．05）。③AHR活化对Treg细胞和Th17细胞分化的影响：AHR激动剂FICZ组的Treg细胞比例明显低于细胞因子组[（2．60±0．40）％,（5．85±0．76）％]（t=4．18,P〈0．01）,但Th17细胞比例升高[（2．86±0．43）％,（1．35±0．08）％]（t=3．65,P〈0．01）。AHR阻断剂白藜芦醇组中的Treg细胞比例和Th17细胞比例均低于细胞因子组,分别为[（0．33±0．14）％,（5．85±0．76）％],（t=7．71,P〈0．01）和[（0．42±0．07）％,（1．35±0．08）％],（t=8．87,P〈0．001）,并且和空白对照组接近,在细胞培养第5天通过7-AAD-AnnexinV对该组细胞检测并未发现细胞异常凋亡或死亡情况,结合该组细胞培养过程中的镜下形态推测该实验组CD4^＋T细胞的分化增殖受到白藜芦醇抑制。结论CSE可促进CD4^＋T细胞向Th17细胞分化,并抑制Treg细胞分化,这一过程可能通过AHR诱导。     

CD+8CD-28T淋巴细胞在肺结核发病机制中的作用

目的 探讨CD8^＋CD28^-T淋巴细胞在肺结核发病机制中的作用。方法 30例病例为2005年3月至5月遵义医学院附属医院呼吸内科住院及门诊患者，采用流式细胞术检测15例肺结核组患者外周血中CD8^＋CD28^-T淋巴细胞比值、细胞内白细胞介素6（IL-6）水平，以及CD3^＋、CD3^＋CD8^＋、CD8^CD28^＋T淋巴细胞比值，15例慢性支气管炎急性发作期患者作为疾病对照组，15名健康人作为健康对照组。结果 肺结核组和疾病对照组CD3^＋T淋巴细胞分别为（41±16）％和（40±10）％，均显著低于健康对照组[（44±6）％]；肺结核组和疾病对照组CD8^＋CD28^＋T淋巴细胞[（47±16）％和（44±10）％]均显著高于健康对照组[（41±12）％]；肺结核组CD8^＋CD28^＋T淋巴细胞[（15±8）％]显著低于疾病对照组[（20±7）％]，两组均显著低于健康对照组[（32±9）％]；肺结核组CD8^＋CD28^-T淋巴细胞[（27±9）％]显著高于疾病对照组[（22±9）％]，两组均显著高于健康对照组[（10±4）％]；肺结核组CD8^＋CD28^-T淋巴细胞分泌的IL-6水平[（32．4±2．4）％]显著高于疾病对照组和健康对照组[（19．7±3．2）％和（15．2±2．7）％]。结论 肺结核患者CD8^＋CD28^-T淋巴细胞及其分泌的IL-6水平在外周血中上调，CD8^＋CD28^＋T淋巴细胞水平在外周血中下调。CD8^＋CD28^＋和CD8^＋CD28^-T淋巴细胞及其分泌的IL-6可能参与肺结核的发病机制。CD8^＋CD28^＋未和CD8^＋CD28^-T淋巴细胞比值及其分泌的IL-6水平可作为活动性肺结核的辅助诊断指标。     

老年人外周血淋巴细胞的凋亡及CD28和CD95的表达

目的通过对健康老年人与健康成年人外周血淋巴细胞的凋亡率及CD28和CD95表达水平的比较性研究,观察衰老对淋巴细胞凋亡的影响,以及CD28和CD95与淋巴细胞凋亡的关系。方法将实验对象分为2组：成年组（25～59岁）与老年组（60～90岁）各20例,采用免疫荧光标记流式细胞术检测外周血淋巴细胞CD28和CD95的水平;Annexin-v-FITC／PI双染色流式细胞术测定地塞米松诱导的淋巴细胞凋亡。结果老年组：淋巴细胞凋亡率[（14．90±4．12）％]显著高于成年组[（8．12±3．12）％];CD28^＋CD95[（8．80±4．86）％]及CD28^＋[（36．31±10．38）％]均明显低于成年组[（23．09±3．48）％、（52．29±4．90）％],而CD28^-CD95^＋[（53．23±8．28）％]、CD95^＋[（80．25±7．19）％]及CD28^-[（63．69±10．38）％]明显高于成年组[（33．58±4．72）％、（63．18±4．12）％、（47．71±4．90）O];CD28^＋CD95^＋在两组间差异无统计学意义。淋巴细胞凋亡率与CD28（CD28^＋）呈负相关,与CD95（CD95^＋）呈正相关。结论老年人淋巴细胞凋亡率上升;CD28^＋表达下降,CD28^-、CD95^＋表达上升;淋巴细胞的凋亡率与CD28^＋、CD95^＋有相关性。提示老化导致老年人淋巴细胞凋亡增加,CD28和CD95的变化与淋巴细胞凋亡密切相关。     

PD-1分子对慢性丙型肝炎患者T细胞免疫功能的影响

目的 探讨慢性丙型肝炎患者外周血T细胞表面程序性死亡因子-1（PD-1）分子在T细胞免疫应答中的作用。方法受试对象包括40例慢性丙型肝炎患者,10例非病毒性肝炎的肝病患者,以及20名健康对照。取外周血,采用流式细胞术检测CD4^＋及CD8^＋T细胞上PD-1的表达水平;ELIsA法测定混合淋巴细胞培养上清中IFN—γ及IL-2的浓度。结果慢性丙型肝炎患者外周血CD4^＋及CD8^＋T细胞上PD-1阳性表达率[（38．61±4．35）％、（48．17±5．16）％]明显高于其他肝病患者及健康对照（P〈0．01）。慢性丙型肝炎患者产生Ⅰ型细胞因子的能力明显降低,阻断PD-1共刺激信号途径能够增强患者T细胞分泌I型细胞因子的能力。结论慢性丙型肝炎患者外周血T细胞上PD-1表达水平的升高,可能是导致T淋巴细胞应答能力下降的重要原因。     

肝癌患者CD8^＋T淋巴细胞穿孔素表达和脱颗粒特点

目的观察肝癌患者外周血CD8^＋T淋巴细胞穿孔紊表达和脱颗粒特点及与临床分期的相关性。方法采集52例肝癌患者、20例健康人的外周血，用流式细胞仪分析CD8^＋T淋巴细胞穿孔素表达百分比；以抗CD3单抗刺激后CD107a表达量代表CD8^＋T淋巴细胞脱颗粒的数量。结果肝癌患者外周血CD8^＋T淋巴细胞穿孔素表达量（32．3％±17．4％）与健康对照（31．8％±14．1％）差异无统计学意义（P〉0．05）。但是抗CD3单抗刺激5h后CD8^＋T淋巴细胞CD107a表达量（6．8％±4．2％）低于健康对照（15．0％±4．3％），差异有统计学意义（P〈0．01）。结论肝癌患者CD8^＋T淋巴细胞脱颗粒能力明显下降。     

CD4^＋CD25^＋调节性T细胞在食管癌中的表达及意义

目的探讨CD4^＋CD25^＋调节性T细胞在食管癌患者免疫失效机制中的作用。方法应用流式细胞仪检测97例食管癌患者外周血和肿瘤组织的CD4^＋CD25^＋调节性T细胞比例,比较不同病理类型、不同分期、有无淋巴结转移患者外周血CD4^＋CD25^＋调节性T细胞的分布变化。结果食管癌患者外周血中CD4^＋CD25^＋调节性T细胞占CD4^＋T淋巴细胞的比例为（17．57±3．99）％,肿瘤组织CD4^＋CD25^＋调节性T细胞比例为（18．97±2．38）％,均高于健康对照组（P均〈0．01）。CD4^＋CD25^＋调节性T细胞比例在不同临床分期、有无淋巴结转移患者间差异有统计学意义（P均〈0．01）。结论食管癌患者全身及肿瘤局部均存在免疫异常,CD4^＋CD25^＋调节性T细胞可能参与了食管癌的发生与发展。     

急性ITP患儿外周血中CD4^＋CD25^＋Foxp3^＋Tr细胞、IL-7水平变化及意义

目的探讨急性特发性血小板减少性紫癜（AITP）的发病机制。方法选择35例AITP患儿（AITP组）和30例健康查体者（对照组）,用流式细胞仪检测外周血CD4^＋CD25^＋Foxp3^＋调节性T（Tr）细胞数量及占CD4^＋细胞比例,ELISA法检测血浆中IL-7水平。结果AITP组和对照组外周血CD4^＋CD25^＋Foxp3^＋Tr细胞／CD;细胞分别为0．11±0．04、0．15±0．02,IL-7分别为（2．32±0．53）、（0．44±0．80）pg／ml,P均〈0．05;AITP组外周血IL-7水平与CD4^＋CD25^＋Foxp3^＋Tr细胞／CD;细胞呈负相关（r=0．71,P〈0．05）。结论CD4^＋CD25^＋Foxp3^＋Tr细胞数量减少、IL-7水平升高可能在AITP发病中具有重要作用,机制为降低有效免疫抑制作用,导致自身反应性T细胞激活增多、凋亡减少,促进血小板破坏。     

抗病毒治疗对慢性丙型肝炎CD4^＋CD25^＋调节性T细胞频率和功能的影响

目的研究抗病毒治疗前后慢性丙型肝炎患者CD4^＋CD25^＋调节性T细胞（Treg）频率和功能的变化。方法筛选HLA—A2阳性慢性丙型肝炎患者31例，给予聚乙二醇化干扰素α-2a（相对分子质量为40000）180μg每周1次皮下注射，联合口服利巴韦林。分别在治疗前和治疗结束随访24周时应用流式细胞仪检测患者CD4^＋CD25^＋ Treg细胞占外周血CD4^＋T细胞的频率，应用液闪计数仪检测其对HCV特异性CD8^＋T细胞增殖的抑制作用，ELISA法检测细胞培养上清γ干扰素（IFN-γ）水平的变化情况。结果治疗结束随访24周，患者外周血CD4^＋CD25^＋ Treg细胞频率为（9．6±3．0）％，明显低于治疗前的（11．0±2．3）％（t=2．028，P〈0．05）；持续病毒学应答（SVR）组CD4^＋CD25^＋ Treg细胞频率为（8．9±2．7）％，明显低于未获得SVR患者组的（10．4±2．3）％（t=3．324，P〈0．01）。抗病毒治疗后CD4^＋CD25^＋ Treg细胞抑制HCV特异性CD8^＋T细胞增殖的作用减弱。治疗后患者IFN-γ水平为（3959±577）pg／ml，明显高于治疗前的（1965±326）pg／ml（t=16．1，P〈0．01）；获得SVR患者组IFN-γ（6824±568）pg／ml，明显高于未获得SVR患者组的（2219±286）pg／ml（t=29．853，P〈0．001）。结论慢性丙型肝炎患者随着HCV RNA水平的下降，CD4^＋CD25^＋Treg细胞频率降低，抑制HCV特异性CD8^＋T细胞增殖的作用减弱。     

Clinical factors affecting rejection rates in liver transplantation

BACKGROUND: With improvements in survival, liver transplant recipients now suffer more morbidity from long-term immunosuppression. Considerations were given to develop individualized immunosuppression based on their risk of rejection. METHOD: We retrospectively analyzed the data of 788 liver transplants performed during the period from October 1991 to December 2011 to study the relationship between acute cellular rejection(ACR) and various clinical factors. RESULTS: Multivariate analysis showed that older age(P=0.04,OR=0.982), chronic hepatitis B virus infection(P=0.005, OR=0.574), living donor liver transplantation(P=0.02, OR=0.648) and use of interleukin-2 receptor antagonist on induction(P0.001, OR=0.401) were associated with fewer ACRs. Patients with fulminant liver failure(P=0.004, OR=4.05) were more likely to develop moderate to severe grade ACR. CONCLUSIONS: Liver transplant recipients with older age,chronic hepatitis B virus infection, living donor liver transplantation and use of interleukin-2 receptor antagonist on induction have fewer ACR. Patients transplanted for fulminant liver failure are at higher risk of moderate to severe grade ACR.These results provide theoretical framework for developing individualized immunosuppression.     

Vitamin D and the risk of acute allograft rejection following human liver transplantation

Background: Vitamin D may act as an immune modulator in experimental and human organ transplantation, but these data are yet to be confirmed in human liver transplantation (LT). Aim: This study aimed to assess the relationship between acute liver allograft cellular rejection (ACR) and pretransplant serum vitamin D concentration or post‐transplant vitamin D supplementation. Method: We studied 133 LT recipients who underwent two per protocol allograft biopsies in the early post‐operative period, plus on‐demand biopsies as clinically indicated. ACR estimate was given according to the Banff scheme in biopsies obtained along two follow‐up periods: (a) from the transplant operation to the end of the second month (0–2 months); (b) and from the third month to the end of the eighth month (3–8 months) post‐LT. Results: The median pretransplant serum 25‐hydroxyvitamin D concentration was 12.5 ng/ml; 40 patients had concentrations ≤12.5 ng/ml, of whom six had ≤5.0 ng/ml. Seventy‐nine recipients received oral vitamin D₃ supplementation to treat post‐transplant osteoporosis. In the 0–2 months period, moderate‐to‐severe rejection episodes were independently associated with cytomegalovirus reactivation (P<0.005) and progressively lower pretransplant serum 25‐hydroxyvitamin D concentrations (P<0.02). Early vitamin D₃ supplementation was independently associated with a lack of ACR (P<0.05). Conclusions: These results suggest that vitamin D may favour immune tolerance towards the liver allograft.     

Should antihepatitis B virus core positive or antihepatitis C virus core positive subjects be accepted as organ donors for liver transplantation?

Since the introduction of liver transplantation as a routine surgical procedure for the treatment of end-stage liver disease, there has been an increasing gap between the number of available grafts and the number of patients on the waiting list. This has led transplant centers to expand the donor pool by different means. One of them has been the introduction of living donor liver transplantation. Other strategies include using less than optimal allografts from deceased donors, the so-called marginal donors, which include the use of grafts from older subjects, livers with moderate amounts of steatosis, or from donors with markers of past or current infection with hepatitis viruses who have absent or minimal liver biochemical or histologic injury. In this review, we will focus on the current use of allografts from donors with antihepatitis B core antibody and/or antibodies against hepatitis C virus in cadaveric and living donor liver transplantation.     

Outcomes of liver transplantation using Hepatitis B core-positive liver grafts: Implications for prophylaxis

The number of patients listed for liver transplantation has outpaced the number of transplants that can be performed. This disparity between transplant candidates and the availability of donor grafts has led to an increase in mortality for patients waiting for liver transplantation. One strategy used to increase the donor pool has been the utilization of expanded donor grafts, such as those from donors with hepatitis B core antibody (anti-HBc). However, use of anti-HBc-positive grafts can potentially place the recipient at risk of de novo post-transplant hepatitis B virus (HBV) infection. The spectrum of liver disease from de novo hepatitis B ranges from mild hepatitis to graft loss. Fortunately, the risk of de novo HBV infection can be decreased with administration of oral nucleosides or nucleotides and hepatitis B immunoglobulin to the recipient. This review focuses on the epidemiology, natural history, and prophylactic strategies to reduce the risk of de novo hepatitis B in liver transplant recipients who receive anti-HBc-positive grafts.     

Immunohistochemical staining of liver grafts with a monoclonal antibody against HCV-Envelope 2 for recurrent hepatitis C after living donor liver transplantation

Aim:  We evaluated the expression of hepatitis C virus (HCV) antigen on liver grafts by immunohistochemical staining (IHS) using IG222 monoclonal antibody (mAb) against HCV-envelope 2 (E2).
Methods:  The study material was 84 liver biopsy specimens obtained from 28 patients who underwent living donor liver transplantation (LDLT) for HCV infection. The biopsy samples were examined histopathologically, and by IHS using IG222 mAb against HCV-E2. Serum HCV-RNA level was measured in all patients. The IHS grades were compared among the three groups classified according to the time elapsed from LDLT (at 1–30, 31–179 and ≥180 days post-LDLT) and among four post-transplant conditions, including acute cellular rejection (ACR).
Results:  Immunoreactivity to IG222 was detected in 78.6% of the specimens obtained during the first month after LDLT, and there were no significant differences on the IHS grades between the three groups classified according to the time elapsed from LDLT. The IHS grades were significantly stronger in definite recurrent HCV ( n  = 12) and probable recurrent HCV ( n  = 7) than in definite ACR ( n  = 7) and other complications ( n  = 8). There were no significant differences in serum HCV-RNA levels among the four post-transplant conditions. There was no significant correlation between the IHS grades using IG222 mAb and serum HCV-RNA levels when data of 84 liver biopsy specimens were analyzed.
Conclusions:  Constant HCV-E2 expression was observed in liver biopsy specimens obtained 1 month or longer. The strong HCV-E2 expression on liver grafts were associated with recurrent hepatitis C after LDLT, but the serum HCV-RNA levels were not.     

肝脏瞬时弹性成像和血清肝纤维化指标对肝移植术后肝纤维化的诊断价值研究

目的评价肝脏瞬时弹性成像(FibroScan)及血清肝纤维化4项[透明质酸(HA)、层粘连蛋白(LN)、Ⅳ型胶原(Ⅳ-C)和血清Ⅲ型前胶原(PCⅢ)]对肝移植患者发生明显肝纤维化(F2)的诊断价值。方法选择2013年2月28日一2014年7月8日在本院治疗的行经皮肝脏穿刺活体组织检查的肝移植和非肝移植慢性肝病患者各40例,进行FibroScan检查以及血清肝纤维化4项检测。将肝脏硬度测定(liver stiffness measurement,LSM)值和血清肝纤维化4项结果与病理检查的肝纤维化程度进行相关性分析,用受试者工作特征曲线(receiver-operating characteristic curve,ROC曲线)分析和评估LSM值和血清肝纤维化4项对肝移植患者明显肝纤维化的诊断价值。结果肝移植患者HA和LSM值与肝纤维化评分呈正相关,r_s分别为0.689和0.782。HA和LSM值诊断肝移植患者明显纤维化的ROC曲线下面积分别为0.789和0.943。明显肝纤维化患者中,肝移植者的LSM值高于非肝移植患者(P0.05);无明显肝纤维化(F≤2)的患者中,肝移植者Ⅳ-C和PCⅢ低于非肝移植患者(P均0.05)。结论 LSM值和血清HA与肝移植患者的肝纤维化评分呈正相关,它们对肝移植患者的明显肝纤维化具有一定的诊断价值。     

Liver grafts from hepatitis B surface antigen-positive donors: A review of the literature

The scarcity of available organs and the gap between supply and demand continue to be the main limitations of liver transplantation. To relieve the organ shortage, current transplant strategies have implemented extended criteria, which include the use of liver from patients with signs of past or present hepatitis B virus (HBV) infection. While the use of liver grafts from donors with evidence of past HBV infection is quite limited, some data have been collected regarding the feasibility of transplanting a liver graft from a hepatitis B surface antigen (HBsAg) positive donor. The aim of the present work was to review the literature regarding liver transplants from HBsAg-positive donors. A total of 17 studies were identified by a search in Medline. To date, HBsAg positive grafts have preferentially been allocated to HBsAg positive recipients. The large majority of these patients continue to be HBsAg positive despite the use of immunoglobulin, and infection prevention can only be guaranteed by using antiviral prophylaxis. Although serological persistence is evident, no significant HBV-related disease has been observed, except in patients coinfected with delta virus. Consistently less data are available for HBsAg negative recipients, although they are mostly promising. HBsAg-positive grafts could be an additional organ source for liver transplantation, provided that the risk of reinfection/reactivation is properly prevented.     

Human mesothelial cells express tissue factor when switched to proliferating state. Pharmacological modulation in vitro.

Covering the inner surface of small-diameter arterial prostheses with endothelial cells (ECs) has been proposed as a means of improving biocompatibility and thrombosis resistance. Because the availability of autologous ECs is limited, autologous human mesothelial cells (HMCs) have been suggested as a substitute for ECs. However, HMCs express tissue factor (TF) in vitro, a deleterious characteristic in vivo. We investigated the distribution of TF antigen and of its inhibitor, tissue factor pathway inhibitor, on HMCs and the effect of pharmacological agents on TF expression. TF antigen was measured by enzyme-linked immunosorbent assay and localized by confocal microscopy. Three distinct pools of TF antigen were demonstrated: within the cells, at the cell surface, and in the extracellular matrix. The effects of ilomedin (10 microg/ml) and heparin (500 U/ml), known to affect procoagulant activity, were evaluated by incubating HMCs for 24 h with or without these agents. Ilomedin, but not heparin, decreased TF antigen expression by 30% (P < 0.05). Despite the theoretical potential of HMCs as a vascular prosthesis lining, TF expression by HMCs remains a major drawback. A technique capable of blocking TF expression until the HMCs return to their resting state is needed. Genetic manipulation of HMCs may hold promise for such a technique.     

Epithelial microchimerism: consistent finding in human liver transplants

BACKGROUND: Eleven liver biopsies from six male patients who received a liver transplant (LT) from female donors were examined in order to determine whether male host-derived hepatic cells were present in female grafts that exhibited minimal or important inflammatory damage. METHODS: Immunohistochemistry for epithelial cell type differentiation (anticytokeratin monoclonal antibody) and fluorescence in situ hybridization for XY chromosomes identification were performed on each slide. RESULTS: Host-derived hepatic cells were found in all except one transplant, with a frequency ranging from 2.3 to 25 per thousand of the total hepatocytes in the biopsy specimen. They were usually found as isolated cells scattered throughout the hepatic lobule; in one patient they were grouped into little clusters. Host-derived hepatic cells persisted throughout the histological follow up (up to 535 days after LT). Polyploidy for XY chromosome was observed. CONCLUSION: Hepatocytes derived from extra-hepatic stem cells are frequently found in small numbers in human liver grafts and persist over time.