移植后淋巴增殖性疾病（PTLD）是移植后最常见的恶性并发症之一，导致患者存活率急剧下降。大多数 PTLD 与 Epstein-Barr 病毒 (EBV PTLD) 密切相关，是 EBV 感染细胞增殖失控的结果。然而，尽管 EBV 感染在移植受者中很常见，但大多数 EBV 载量高的患者永远不会发展为 EBV PTLD。自然杀伤细胞和 EBV 特异性 CD8 T 淋巴细胞对于控制 EBV 感染细胞至关重要，这些细胞毒性免疫反应的损害促进 EBV 感染细胞不受限制的增殖。近年来，旨在描述与 EBV PTLD 发生相关的新危险因素的现有文献显着增加，这些因素可能与 EBV 特异性自然杀伤细胞和 EBV-CD8 T 淋巴细胞反应的强度密切相关。风险因素的积累和发生 EBV PTLD 风险的增加是相辅相成的。一方面，大多数风险因素，例如免疫抑制水平或 EBV 供体和受体血清学不匹配，以及不同的遗传风险因素与宿主相关，并影响细胞毒性 EBV 特异性免疫反应。另一方面，越来越多的证据表明，不同的 EBV 变异可能具有增加的恶性潜力，因此更有可能诱发 EBV PTLD。在这里，我们旨在从机制的角度回顾宿主体内 EBV PTLD 的危险因素以及感染 EBV 变异体，这些变异体可以解释为什么只有少数移植受者会出现 EBV PTLD。版权所有 © 2024 Wolters Kluwer Health, Inc 。 版权所有。

Posttransplant lymphoproliferative disorders (PTLDs) are among the most common malignant complications after transplantation, leading to a drastic reduction in patient survival rates. The majority of PTLDs are tightly linked to Epstein-Barr virus (EBV+PTLDs) and are the result of an uncontrolled proliferation of EBV-infected cells. However, although EBV infections are a common finding in transplant recipients, most patients with high EBV loads will never develop EBV+PTLD. Natural killer cells and EBV-specific CD8+ T lymphocytes are critical for controlling EBV-infected cells, and the impairment of these cytotoxic immune responses facilitates the unfettered proliferation of EBV-infected cells. Recent years have seen a considerable increase in available literature aiming to describe novel risk factors associated with the development of EBV+PTLD, which may critically relate to the strength of EBV-specific natural killer cell and EBV-CD8+ T lymphocyte responses. The accumulation of risk factors and the increased risk of developing EBV+PTLD go hand in hand. On the one hand, most of these risk factors, such as the level of immunosuppression or the EBV donor and recipient serologic mismatch, and distinct genetic risk factors are host related and affect cytotoxic EBV-specific immune responses. On the other hand, there is growing evidence that distinct EBV variants may have an increased malignant potential and are thus more likely to induce EBV+PTLD. Here, we aim to review, from a mechanistic point of view, the risk factors for EBV+PTLD in the host and the infecting EBV variants that may explain why only a minority of transplant recipients develop EBV+PTLD.Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.