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Article(id=1276203025333092768, tenantId=1146029695717560320, journalId=1146031591421210625, issueId=1276202956391313894, articleNumber=null, orderNo=null, doi=10.3981/j.issn.1000-7857.2025.06.00058, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1749052800000, receivedDateStr=2025-06-05, revisedDate=1766505600000, revisedDateStr=2025-12-24, acceptedDate=null, acceptedDateStr=null, onlineDate=1782200111945, onlineDateStr=2026-06-23, pubDate=1781280000000, pubDateStr=2026-06-13, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782200111945, onlineIssueDateStr=2026-06-23, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782200111945, creator=13701087609, updateTime=1782200111945, updator=13701087609, issue=Issue{id=1276202956391313894, tenantId=1146029695717560320, journalId=1146031591421210625, year='2026', volume='44', issue='11', pageStart='1', pageEnd='136', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782200095507, creator=13701087609, updateTime=1782200147766, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1276203176344810276, tenantId=1146029695717560320, journalId=1146031591421210625, issueId=1276202956391313894, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276203176344810277, tenantId=1146029695717560320, journalId=1146031591421210625, issueId=1276202956391313894, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=33, endPage=41, ext={EN=ArticleExt(id=1276203025861575074, articleId=1276203025333092768, tenantId=1146029695717560320, journalId=1146031591421210625, language=EN, title=New strategies for the prevention and treatment of immune injury in liver transplantation, columnId=1150494642224591153, journalTitle=Science & Technology Review, columnName=Exclusive, runingTitle=null, highlight=null, articleAbstract=

Liver transplantation is the only effective treatment for various end−stage liver diseases. However, immune injury after liver transplantation, such as acute rejection (AR), chronic rejection (CR), hepatic ischemia−reperfusion injury (HIRI), and opportunistic infection, still seriously affects the prognosis of patients. Although great progress has been made in the research of immune injury after liver transplantation, there are still many deficiencies in clinical practice. In this article, the functional changes of hepatocytes and non−parenchymal cells after liver transplantation were used as the breakthrough point to summarize and clarify the potential molecular mechanisms of immune injury after liver transplantation, systematically review the latest progress in the prevention and treatment of immune injury after liver transplantation, and focus on emerging prevention and treatment strategies and their clinical application prospects. The application of artificial intelligence and big data technology in the prediction, diagnosis, treatment and management of immune injury in liver transplantation is prospected, in order to provide reference for related basic research and clinical application.

, correspAuthors=Yanyao LIU, authorNote=null, correspAuthorsNote=null, copyrightStatement=All rights reserved. Unauthorized reproduction is prohibited., copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, authorCompany=null, fund=null, authors=null, authorsList=Zhengli TAN, Qiang LIU, Yanyao LIU), CN=ArticleExt(id=1276203027048563110, articleId=1276203025333092768, tenantId=1146029695717560320, journalId=1146031591421210625, language=CN, title=肝移植免疫损伤防治新策略, columnId=1150494642375586098, journalTitle=科技导报, columnName=特色专题, runingTitle=null, highlight=null, articleAbstract=

肝移植是各种终末期肝病的唯一有效治疗手段，但肝移植术后免疫损伤，例如急性排斥反应（acute rejection，AR）、慢性排斥反应（chronic rejection，CR）、肝缺血再灌注损伤（hepatic ischemia−reperfusion injury，HIRI）、机会性感染等仍严重影响患者预后。虽然目前对肝移植免疫损伤的研究已经取得很大进展，但临床实践中仍存在许多不足。以肝移植后肝实质细胞和非实质细胞功能变化为切入点，总结并阐明肝移植术后免疫损伤的潜在分子机制，并系统梳理肝移植免疫损伤防治最新进展：在急性排斥反应方面，正在开展新型免疫抑制剂和生物制剂的临床试验；在缺血再灌注损伤方面，研究重点扩展到调控特定肝脏实质和非实质细胞；离体器官保存技术方面，提出了低温/常温机械灌注和无缺血移植理念；在术后机会性感染的防治方面，通过优化个体化免疫抑制方案进而实现精确治疗。聚焦新兴防治策略及其临床应用前景，对人工智能和大数据技术在肝移植免疫损伤的预测、治疗和管理作出展望，提出通过集成患者的生理参数、实验室检查结果、药物使用情况、影像学资料以及可穿戴设备数据等多源信息，可以构建“智慧病房”监测系统，以期为相关基础研究和临床应用提供参考。

, correspAuthors=刘彦尧, authorNote=null, correspAuthorsNote=
刘彦尧（通信作者），副研究员，研究方向为肝移植术后缺血再灌注损伤，电子信箱：
, copyrightStatement=版权所有，未经授权，不得转载。, copyrightOwner=《科技导报》编辑部, extLink=null, articleAbsUrl=null, sourceXml=9vUwuOmbymzTykSZH7DAWg==, magXml=Ql2cl9t4ZcWWs7g6k2krqg==, pdfUrl=null, pdf=4SsreWdOkuwqCxNC5gpxCA==, pdfFileSize=938082, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=vU3hFeYTiIdYm0AJMc8jrA==, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=6K7WYS55p2R9FSekG2/i6Q==, mapNumber=null, authorCompany=null, fund=null, authors=

谭政立，硕士研究生，研究方向为肝移植术后缺血再灌注损伤，电子信箱：

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谭政立，硕士研究生，研究方向为肝移植术后缺血再灌注损伤，电子信箱：

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谭政立，硕士研究生，研究方向为肝移植术后缺血再灌注损伤，电子信箱：

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肝移植免疫损伤防治新策略
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谭政立 , 刘强 , 刘彦尧 *
科技导报 | 特色专题 2026,44(11): 33-41
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科技导报 | 特色专题 2026, 44(11): 33-41
肝移植免疫损伤防治新策略
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谭政立 , 刘强, 刘彦尧*
作者信息
  • 重庆医科大学附属第一医院肝胆外科，重庆 400016

    • 谭政立，硕士研究生，研究方向为肝移植术后缺血再灌注损伤，电子信箱：

通讯作者:

刘彦尧（通信作者），副研究员，研究方向为肝移植术后缺血再灌注损伤，电子信箱：
New strategies for the prevention and treatment of immune injury in liver transplantation
Zhengli TAN , Qiang LIU, Yanyao LIU*
Affiliations
  • Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
出版时间: 2026-06-13 doi: 10.3981/j.issn.1000-7857.2025.06.00058
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摘要
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肝移植是各种终末期肝病的唯一有效治疗手段，但肝移植术后免疫损伤，例如急性排斥反应（acute rejection，AR）、慢性排斥反应（chronic rejection，CR）、肝缺血再灌注损伤（hepatic ischemia−reperfusion injury，HIRI）、机会性感染等仍严重影响患者预后。虽然目前对肝移植免疫损伤的研究已经取得很大进展，但临床实践中仍存在许多不足。以肝移植后肝实质细胞和非实质细胞功能变化为切入点，总结并阐明肝移植术后免疫损伤的潜在分子机制，并系统梳理肝移植免疫损伤防治最新进展：在急性排斥反应方面，正在开展新型免疫抑制剂和生物制剂的临床试验；在缺血再灌注损伤方面，研究重点扩展到调控特定肝脏实质和非实质细胞；离体器官保存技术方面，提出了低温/常温机械灌注和无缺血移植理念；在术后机会性感染的防治方面，通过优化个体化免疫抑制方案进而实现精确治疗。聚焦新兴防治策略及其临床应用前景，对人工智能和大数据技术在肝移植免疫损伤的预测、治疗和管理作出展望，提出通过集成患者的生理参数、实验室检查结果、药物使用情况、影像学资料以及可穿戴设备数据等多源信息，可以构建“智慧病房”监测系统，以期为相关基础研究和临床应用提供参考。

肝移植  /  免疫损伤  /  急性排斥反应  /  缺血再灌注损伤  /  免疫细胞

Liver transplantation is the only effective treatment for various end−stage liver diseases. However, immune injury after liver transplantation, such as acute rejection (AR), chronic rejection (CR), hepatic ischemia−reperfusion injury (HIRI), and opportunistic infection, still seriously affects the prognosis of patients. Although great progress has been made in the research of immune injury after liver transplantation, there are still many deficiencies in clinical practice. In this article, the functional changes of hepatocytes and non−parenchymal cells after liver transplantation were used as the breakthrough point to summarize and clarify the potential molecular mechanisms of immune injury after liver transplantation, systematically review the latest progress in the prevention and treatment of immune injury after liver transplantation, and focus on emerging prevention and treatment strategies and their clinical application prospects. The application of artificial intelligence and big data technology in the prediction, diagnosis, treatment and management of immune injury in liver transplantation is prospected, in order to provide reference for related basic research and clinical application.

liver transplantation  /  immune damage  /  acute rejection  /  ischemia−reperfusion injury  /  immune cells
谭政立, 刘强, 刘彦尧. 肝移植免疫损伤防治新策略. 科技导报, 2026 , 44 (11) : 33 -41 . DOI: 10.3981/j.issn.1000-7857.2025.06.00058
Zhengli TAN, Qiang LIU, Yanyao LIU. New strategies for the prevention and treatment of immune injury in liver transplantation[J]. Science & Technology Review, 2026 , 44 (11) : 33 -41 . DOI: 10.3981/j.issn.1000-7857.2025.06.00058
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肝移植是各种终末期肝病的唯一有效治疗手段[1]。尽管肝移植手术趋于成熟，移植患者围手术期管理逐渐完善，但与免疫系统状态密切相关的术后并发症仍是影响患者长期生存的关键因素。这既包括由免疫系统过度激活或识别介导的移植物组织损伤，如急性排斥反应（AR）、慢性排斥反应（CR）、肝缺血再灌注损伤（HIRI）中的免疫炎症反应，也包括因长期免疫抑制导致免疫防御功能缺失而引发的机会性感染[2−3]。虽然目前对肝移植免疫损伤的研究已经取得一定进展，但其具体机制尚不清楚。因此，探究新型免疫损伤防治策略已成为当务之急。系统梳理了肝移植免疫损伤防治的相关研究进展，聚焦新兴防治策略及其临床应用前景，以期为基础研究和临床应用提供参考。
1 急性排斥反应
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肝移植后AR是指受体免疫系统对同种异体移植肝脏进行免疫识别，进而通过细胞免疫和体液免疫应答介导移植物组织损伤及功能障碍的病理生理过程[4]。AR的临床表现多样，可包括发热、移植肝肿大、肝功能异常、肝区压痛、黄疸和胆汁分泌障碍等[5]。
既往研究指出，T淋巴细胞是AR的核心效应细胞和调节细胞，其中Th17细胞不仅可以促进同种异体移植物排斥反应，还可以激活Th1、Th2和CD8+T细胞等来加重炎症反应[6]。调节性T细胞（regulatory T cells, Treg）是一组抑制免疫反应并维持免疫稳态和自我耐受性的T细胞，Th17与Treg分化之间存在动态平衡。一项研究指出，使用Treg的抗CD25抗体治疗的免疫耐受小鼠在同种异体移植模型后发生了Treg/Th17细胞比率降低相关的排斥反应[7]。围移植期使用Treg细胞疗法可以减少供体特异性同种异体反应，并有助于免疫抑制剂的早期停用[8]。调节性B细胞（regulatory B cells，Breg）与Treg细胞发挥着类似的作用，南京医科大学附属第一医院的团队研究发现，肝移植术后发生AR的患者中，循环血流中的记忆型Breg细胞比例显著下降，且免疫抑制功能受到损害。此外，该团队还进一步揭示miR−29a−3p是记忆型Bregs细胞分化的关键调控因子，沉默miR−29a−3p可能通过调控记忆型Bregs细胞分化继而诱导供肝免疫耐受[9]。肝巨噬细胞（kupffer cells，KCs）是固有免疫的关键效应细胞，在AR的发生发展中扮演既促炎又抑炎的双重角色，活化的M1型KCs会产生大量促炎细胞因子和趋化因子，招募和激活其他免疫细胞，放大炎症反应，导致组织损伤；而M2型KCs主要发挥抗炎和组织修复作用[10]。因此，促进KCs向M2型转化是减轻AR的有效干预策略。树突状细胞（dendritic cells，DCs）是最重要的专职抗原呈递细胞，在启动和调节适应性免疫应答中发挥核心作用[11]。使用供体或宿主来源的致耐受性DCs或原位靶向DCs进行细胞治疗以促进其耐受性是一种新兴方法，可以减少移植患者全身性免疫抑制剂的使用并促进供体特异性耐受性[12]。
AR的精确治疗旨在通过个体化的治疗方案，在有效控制排斥反应的同时，最大限度地减少免疫抑制剂的相关副作用，提高移植物和患者的长期存活率，目前的有效手段包括研发新型免疫抑制药物、优化药物联合应用方案和研发精准的AR预测模型。传统免疫抑制剂，如钙调神经磷酸酶抑制剂（calcineurin inhibitors，CNIs）、糖皮质激素和麦考酚酸酯（mycophenolate mofetil，MMF）等在预防和治疗AR方面取得了巨大成果，但也伴随着肾毒性、神经毒性、代谢紊乱、感染和肿瘤风险增加等副作用[13]。JAK激酶是多种细胞因子和生长因子受体下游信号转导通路的关键组成部分，参与免疫细胞的活化和功能调节。JAK抑制剂如托法替尼、巴瑞替尼和乌帕替尼等，通过抑制JAK/STAT信号通路从而发挥免疫抑制作用。在实体器官移植领域，JAK抑制剂已显示出改善移植物功能、降低AR发生率及严重程度、下调促炎细胞因子和黏附分子表达以及减少氧化应激的潜力[14]。然而，JAK抑制剂在肝移植AR防治中的大型临床试验数据尚有限，其远期疗效和安全性仍需进一步评估。鞘氨醇−1−磷酸受体（sphingosine−1−phosphate，S1P）调节剂及其受体在淋巴细胞迁移、活化和存活中发挥重要作用。S1P受体调节剂如芬戈莫德、奥扎莫德、西尼莫德和泊奈莫德等通过作用于淋巴细胞表面的S1P1受体，阻止淋巴细胞外流，从而减少外周血淋巴细胞数量，发挥免疫抑制作用。这类药物已在大鼠心脏移植模型中显示出了预防排斥反应的潜力，将其运用于肝移植领域，可能是缓解AR的一个重要策略[15]。为了在有效预防AR的同时减少单一药物大剂量使用带来的毒副作用，联合免疫抑制治疗是目前临床的标准策略。多项研究表明，早期（如术后1个月）或晚期（维持期）引入mTOR抑制剂并减少CNIs剂量，可以在不增加AR风险的前提下，显著改善受者肾功能，并降低肝癌肝移植术后肿瘤复发风险[16]。
传统的AR诊断主要依赖于肝功能生化指标监测和有创的肝活检病理学检查，后者仍是诊断移植术后AR的金标准，但存在取样误差、操作风险和评估滞后性等问题。因此，开发无创、高灵敏度、高特异性的新型生物标志物，用于AR的预测、早期诊断和免疫状态监测，对实现个体化精准治疗至关重要[17]。匹兹堡大学肝移植研究中心开发了一种基于外周血基因表达的生物标志物（包括36种基因探针模型），实现了区分AR与其他原因导致的肝功能异常，并能在AR相关的移植物损伤发生前检测到早期信号，有望实现AR的早期诊断[18]。供体来源的游离DNA（donor−derived cell−free DNA, dd−cfDNA）是来源于受损或凋亡的供肝细胞释放到受者外周血中的DNA片段，报道指出dd−cfDNA水平在AR发生时显著升高，且比传统肝功能指标的变化更灵敏，具有较高的诊断和预测价值[19]。miRNAs是一类内源性非编码小RNA，通过调控靶基因表达参与多种生理病理过程，包括免疫应答和排斥反应。血清或血浆中特定miRNAs的表达谱改变与AR密切相关[20]。Muthukumar等[21]发现一个包含9个miRNAs的组合（包括miR−210、miR−194、miR−34a、miR−192、miR−885、miR−193）能够诊断AR，其中miR−210和miR−34a的组合模型能正确区分所有活检样本。这些新型药物干预靶点和预测靶标的探索和临床验证，将有助于实现AR的早期预警、精准诊断和个体化治疗，从而改善肝移植患者的预后。然而，大部分相关内容仍处于临床前研究阶段，其临床应用的安全性、可靠性和成本效益仍需大规模、多中心的临床试验进行验证。
2 缺血再灌注损伤
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肝移植HIRI是指供肝在肝移植过程中经历缺血缺氧后恢复血流时所发生的损伤，通常包含缺血损伤和再灌注损伤2个阶段[22]。严重的HIRI可导致原发性移植物无功能、早期移植物功能不良，增加急性排斥反应、胆道并发症、感染等术后并发症的发生风险，并影响远期移植物存活率和患者生存率[23]。
HIRI包含了钙超载、氧化应激损伤、酸中毒、补体激活等复杂病理过程，肝细胞、肝窦内皮细胞（liver sinusoidal endothelial cells, LSECs）以及部分免疫细胞都在HIRI的发生和发展中扮演了关键角色（图1）。肝细胞作为肝脏主要代谢枢纽，参与糖、脂肪和蛋白质代谢，对缺血缺氧高度敏感，是HIRI影响的关键靶细胞之一。缺血期，肝细胞线粒体功能障碍导致细胞能量代谢紊乱，当再灌注时线粒体呼吸链功能障碍诱导活性氧（reactive oxygen species，ROS）大量产生并引发氧化应激损伤[24]。因此，减少氧化应激和改善线粒体功能障碍是改善肝移植后HIRI的关键策略之一。N−乙酰半胱氨酸（N−Acetylcysteine, NAC）和Mito−TEMPO是2种有前景的抗氧化剂，临床研究已证实它们可以通过减少氧化应激反应从而预防肝损伤[25−26]。一项荟萃分析显示，围手术期内对供体和（或）受体应用NAC可减少肝移植术后并发症的发生，改善肝酶水平并提升移植物存活率[27]。与非靶向抗氧化剂相比，Mito−TEMPO特异性靶向作用于线粒体，可以最大限度地减少由HIRI导致的细胞内ROS堆积。HIRI过程中，肝细胞可发生多种形式的死亡，包括坏死、凋亡、坏死性凋亡、焦亡和铁死亡等[28]。铁死亡是移植物中显著存在的程序性细胞死亡形式，近年来逐渐成为研究热点。中山大学附属第三医院团队研究发现高龄供肝在HIRI中表现出更为严重的损伤，其机制主要与FTO基因过表达相关。烟酰胺单核苷酸可以上调FTO的去甲基化活性，通过ACSL4/TFRC通路进一步抑制铁死亡以减轻高龄供肝HIRI[29]。花生四烯酸15−脂氧合酶−1（arachidonic acid 15−lipoxygenase−1，ALOX15）和诱导型一氧化氮合酶（inducible nitric oxide synthase，iNOS）近期被发现是干预肝移植引发HIRI的潜在靶点，黄芩素可能通过调节ALOX15和iNOS介导的铁死亡，在HIRI中发挥保护作用[30]。有团队研究发现，二甲双胍可通过重塑肠道菌群丰度调控γ−氨基丁酸代谢抑制铁死亡从而缓解HIRI[31]。Lachnospiraceae−bacterium菌衍生的丙酮酸能抑制FOXO3和ALOX15的表达，从而减少正常和脂肪供肝的炎症和铁死亡，这揭示了肠道菌群与铁死亡的潜在关联[32]。LSECs是构成肝血窦内壁的特殊内皮细胞，具有独特的窗孔结构，在维持肝脏微循环、物质交换、免疫调节和清除血液中大分子等方面发挥着关键作用。在HIRI期间，LSECs肿胀、窗孔丢失或形成大的间隙，血窦屏障功能受损[33]。LSECs的修复对肝脏整体功能的恢复至关重要，研究表明，KCs通过VEGF−A/VEGFR1信号和EGF产生促进LSECs修复和血窦重建[34]。因此，针对LSECs修复的信号通路是一种潜在的治疗方法。中性粒细胞在再灌注后迅速被激活的KCs和受损肝细胞释放的趋化因子吸引至肝脏，激活并释放中性粒细胞胞外诱捕网（neutrophil extracellular traps, NETs）。NETs是由DNA、组蛋白、弹性蛋白酶和髓过氧化物酶等组成的网状结构，在无菌性炎症中，除了捕获病原体外，还会造成严重的组织损伤[35]。DNase−1可以通过降解NETs的DNA骨架，进而减少NETs的生成，姜黄素与DNase−1联合使用在减轻HIRI方面效果更显著[36]。肽酰精氨酸脱亚氨酶4（peptidylarginine deiminase 4, PAD4）是NETs形成过程中组蛋白瓜氨酸化和染色质去凝集所必需的酶，PAD4抑制剂可以抑制大鼠肝移植缺血再灌注损伤模型供肝中NETs形成，进而缓解HIRI[37]。
供肝在获取后至植入受体前，需要经过离体保存并完成转运，传统的保存方法是静态冷藏（static cold storage，SCS），即将供肝置于0~4℃的器官保存液中，低温可以降低供肝内肝细胞代谢率，减轻肝损伤。然而供肝在低温冷藏过程中肝细胞损伤难以避免，且SCS无法对供肝功能进行评估和修复。特别是对于边缘供肝，如心脏死亡捐献者（donation after cardiac death，DCD）供肝、脂肪供肝和老年供肝等，SCS对其保护效果不佳，移植后HIRI和并发症风险较高[38]。
为克服SCS的局限，机械灌注（machine perfusion，MP）技术应运而生，它通过持续的脉动或非脉动灌注来模拟生理环境。目前主流的MP策略主要包括低温和常温2大类。低温氧合机械灌注（hypothermic oxygenated machine perfusion，HOPE）及双低温氧合灌注（dual hypothermic oxygenated perfusion，DHOPE）是指在低温（通常4~12℃）条件下，通过门静脉或/和肝动脉灌注富氧保存液，从而保护供肝功能[39]。一项纳入7项随机对照试验的分析显示，HOPE能改善移植物存活率，减少扩展标准供肝的严重不良事件，并降低DCD肝移植后缺血性胆道并发症的发生率[40]。国外的一项回顾性研究探讨了延长供肝HOPE/DHOPE灌注时间的可行性和益处，发现延长灌注时间安全可靠，有助于改善移植后HIRI，并可能降低术后急性肾损伤的风险，即使针对边缘供肝也能获得良好预后[41]。常温机械灌注（normothermic machine perfusion，NMP）是指在接近生理体温（35~37℃）的条件下，使用基于血液或含氧载体的灌注液灌注供肝，以维持供肝的正常生理代谢功能，包括合成蛋白质、产生胆汁、清除乳酸等[39]。NMP同样被证明优于SCS，尤其在提高边缘供肝利用率方面潜力巨大。一项随机对照试验显示，NMP可使移植物损伤率和器官丢弃率降低50%，NMP期间监测灌注液中的乳酸水平、胆汁产生量、灌注液pH和血管阻力等参数，可以作为评估肝脏活力的重要指标[42]。
基于NMP技术的进一步革新，催生了“无缺血肝移植”（ischemia−free liver transplantation, IFLT）这一创新理念。旨在通过从供体器官获取到受体植入全程维持器官血流灌注，最大限度避免缺血和再灌注损伤。一项关于IFLT的随机对照试验（randomized controlled trial, RCT）报道指出，与传统方法相比，IFLT大幅减少了供肝移植术后胆道狭窄和早期移植物功能障碍等HIRI相关并发症的发生率[43]。尽管目前IFLT技术复杂且成本较高，IFLT仍代表了离体器官保存的未来发展方向之一，有望显著改善移植预后，特别是对于DCD和脂肪变性等高缺血损伤易感性供肝而言，IFLT的应用优势明显。
除灌注技术的革新之外，器官保存液的改良也在不断探索中。目前临床常用的静态冷保存液主要包括威斯康星大学保存液、组氨酸−色氨酸−酮戊二酸溶液（HTK液）和Celsior液等[44]。HTK−N溶液是HTK溶液的改良版，通过部分或完全以N−乙酰−L−组氨酸替代组氨酸，并添加铁螯合剂、L−精氨酸，以及补充天冬氨酸和α−酮戊二酸作为三羧酸循环底物，旨在抑制羟自由基生成、改善能量代谢、减轻细胞水肿[45]。临床前研究显示，其在减轻供肝储存的冷藏损伤方面明显优于HTK，Ⅱ期临床试验已证实其在肾移植中的安全性和有效性，其在肝移植领域的应用价值仍有待进一步研究和临床试验[46]。
上述这些新型器官保存技术，特别是MP，正在逐步改变肝移植的临床实践，有望显著改善边缘供肝的利用率和移植预后。
3 术后机会性感染
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肝移植受者术后因长期、大剂量使用免疫抑制剂致机体免疫功能低下，极易并发各种机会性感染，严重影响患者预后。
对于因乙型肝炎病毒（HBV）相关肝病接受肝移植的患者，尤其是在中国等HBV高流行区，术后HBV复发构成严峻挑战。免疫抑制状态下，潜伏的HBV可被再激活，可致移植肝再次发生肝炎、肝硬化甚至肝癌[47]。有效的抗病毒预防方案，如核苷（酸）类似物（nucleos（t）ide analogs, NAs）联合或不联合乙型肝炎免疫球蛋白（hepatitis B immunoglobulin，HBIG），是控制HBV复发的关键。一项国内双中心研究提示，HBV再激活与移植后肝细胞肝癌复发高度相关[48]。此外，微血管浸润和HBsAg阳性是独立于Milan标准的HBV再激活危险因素，并据此建立了具有良好预测效能的受试者工作曲线[48]。理论上，对于采取有效抗病毒方案后产生抗体的应答者，停止包括NAs在内的联合预防措施具有可行性。此前已有研究证实，应答者在产生足够滴度的乙肝表面抗体后，停止长期注射HBIG是可行和安全的[49]。所有应答者于接种后平均12~14个月停止注射HBIG，随访期内未见HBV再激活。然而，目前尚缺乏免疫重建后停用HBIG的长期随访结果，此方面仍有待大样本临床研究进一步探讨。
巨细胞病毒（cytomegalovirus，CMV）感染是肝移植术后最常见的机会性病毒感染之一，可导致CMV病，并增加排斥反应、其他机会性感染和移植物失功的风险[50]。目前，CMV的IgG血清学是移植前供受体筛查的标准方法。尽管预防策略降低了CMV病的风险，但其在术后肝移植患者中的感染率仍高达55.7%[51]。莱特莫韦是新型抗CMV药物，相比于传统药物，其具有更好的安全性。莱特莫韦已在造血干细胞移植中用于预防CMV感染，其在实体器官移植（包括肝移植）中的研究正在进行中[52]。
在肝移植领域，控制术后机会性感染的关键在于优化免疫抑制方案，实现“既有效预防排斥反应，又最大限度降低感染风险”的平衡。青海大学移植团队开发了肝移植受者术后多重耐药微生物感染的风险模型，有利于早期发现潜在危险进而实行精确免疫治疗[53]。通过个体化调整免疫抑制方案、合理应用新型免疫抑制剂、结合先进的免疫功能和病原学监测技术，以及针对特定病原体开发新的防治策略，有望进一步降低肝移植术后机会性感染的发生率和病死率，改善患者预后。
4 慢性排斥反应
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肝移植CR是指以免疫介导的进行性胆管损伤和血管病变为主要特征的移植物损伤，最终导致胆管缺失和闭塞性动脉病，并由此引发胆汁淤积、肝纤维化、肝硬化及移植物功能衰竭[54]。CR是肝移植术后远期重要并发症之一，CR进展到晚期常不可逆，再次肝移植是晚期CR的唯一有效的治疗手段。近年来的研究指出，mTOR抑制剂（西罗莫司、依维莫司）除免疫抑制作用外，还具有抗肝纤维化和抗血管增生的潜力，有益于伴有供肝血管病变的CR防治。一项临床试验对23例经活检证实的CR患者采用“挽救疗法”，即在基础免疫抑制方案中加用mTOR抑制剂治疗肝移植后CR，结果显示，12例（52%）患者CR成功逆转，其余患者预后不良，多需再次移植。上述研究表明，mTOR抑制剂附加疗法在T细胞介导的慢性排斥反应（T–cell mediated chronic rejection，TCMCR）治疗中或具应用价值，值得进一步探索[55]。
尽管CR的防治仍面临挑战，但随着对其发病机制认识的不断深入，以及新型免疫抑制剂、生物制剂、细胞治疗和靶向药物的研发，未来有望涌现出更有效的防治策略，以进一步改善肝移植患者的长期预后。
5 展望
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肝移植免疫损伤的防治是提高移植长期存活率和改善患者生活质量的核心环节。未来，随着基础医学、临床医学、生物技术以及信息科学的飞速发展，肝移植免疫损伤的防治策略将日趋精准化、个体化和智能化。
通过集成患者的生理参数、实验室检查结果、药物使用情况、影像学资料以及可穿戴设备数据等多源信息，可以构建“智慧病房”监测系统。人工智能（artificial intelligence，AI）算法可以实时分析这些数据，动态评估患者的免疫状态和移植物功能，从而早期预测肝移植免疫损伤（如AR、HIRI加重）的发生风险。例如，通过机器学习模型分析连续监测的生物标志物（如dd−cfDNA、miRNA）变化趋势并结合临床症状，可实现对排斥反应的早期预警。AI还可以辅助临床医师根据患者个体反应及预测的排斥/感染风险，动态优化治疗方案，实现肝移植患者术后免疫抑制剂的个体化应用。目前已有临床试验探索AI指导下的肝移植术后他克莫司的应用，并在改善药物浓度达标率方面展现出治疗潜力[56−57]。整合基因组学、转录组学、蛋白质组学、代谢组学、微生物组学等多组学大数据，结合临床表型数据，构建肝移植免疫损伤的综合数据库，AI算法也可用于分析此类高维复杂的多组学数据，以识别与特定免疫损伤类型（AR、CR和HIRI）相关的新型分子标志物、信号通路及潜在治疗靶点。
6 结论
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肝移植是终末期肝病和部分肝癌患者获得长期生存的有效手段。然而，术后免疫损伤，包括AR、CR、HIRI以及免疫抑制相关的机会性感染（尤其是HBV复发），仍然是影响移植预后的主要挑战。近年来，随着对肝移植免疫损伤机制认识的不断深化，其防治策略取得了显著进展。在AR方面，针对不同免疫细胞亚群的治疗新靶点研究方兴未艾，有关新型免疫抑制剂和生物制剂的临床试验正在积极开展，基于组学和液体活检的无创监测技术为早期诊断和个体化治疗提供了可能。在HIRI方面，研究重点从关注的抗炎、抗氧化治疗扩展到调控特定肝脏实质和非实质细胞，离体器官保存技术的革新特别是低温/常温机械灌注和无缺血移植理念的提出与实践以及新型器官保存液的研发，为减轻HIRI、改善供肝质量带来了希望。在术后机会性感染的防治方面，尤其关注HBV复发和肝癌复发的问题。通过优化个体化免疫抑制方案进而实现精确治疗，在抑制排斥的同时降低感染的风险。CR的机制复杂，涉及细胞和体液免疫的持续作用，导致胆管消失和闭塞性动脉病。目前治疗手段有限，重点在于优化长期免疫抑制管理，并探索细胞治疗等新型干预措施。展望未来，AI和大数据技术将在肝移植免疫损伤的预测、诊断、治疗和管理中发挥日益重要的作用。随着基础研究的深入和临床试验的持续推进，肝移植免疫损伤的防治策略必将不断完善，为更多肝移植患者带来更长久、更高质量的生命。
基金
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  • 国家自然科学基金青年科学基金项目(82300745)
  • 国家自然科学基金面上项目(82570779)
  • 国家级大学生创新训练计划(202410631017)
文献
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2026年第44卷第11期
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doi: 10.3981/j.issn.1000-7857.2025.06.00058
  • 接收时间：2025-06-05
  • 首发时间：2026-06-23
  • 出版时间：2026-06-13
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  • 收稿日期：2025-06-05
  • 修回日期：2025-12-24
基金
国家自然科学基金青年科学基金项目(82300745)
国家自然科学基金面上项目(82570779)
国家级大学生创新训练计划(202410631017)
作者信息
    重庆医科大学附属第一医院肝胆外科，重庆 400016

通讯作者:

刘彦尧（通信作者），副研究员，研究方向为肝移植术后缺血再灌注损伤，电子信箱：
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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