免疫衰老与肝移植术后感染:从生物学机制到临床预后的深度评估
Immune Aging and Post-Liver Transplant Infection: A Comprehensive Assessment from Biological Mechanisms to Clinical Outcomes
摘要: 肝移植术后感染是影响受者长期生存的主要障碍。近年研究发现,免疫衰老——以衰老相关分泌表型(SASP)驱动的炎性衰老、髓系偏移及肠道菌群失调为特征——是决定术后感染易感性与移植物预后的关键因素。在肝移植受者中,该过程受供肝年龄、缺血再灌注损伤及长期免疫抑制共同加剧,表现为CD4+T细胞与NK细胞重建延迟、T细胞受体多样性降低及代谢重塑。临床研究证实,免疫衰老状态与多重耐药菌感染、潜伏病毒再激活及严重脓毒症风险显著相关,血清IL-6、TNF-α等炎症标志物可作为预测感染严重程度和生存率的独立指标。针对性地清除衰老细胞、调控肠道微生态、阻断特定炎症通路及优化免疫策略,有望重建受者免疫稳态。未来将免疫衰老标志物整合至临床风险评估体系,对实现肝移植术后个体化感染防控具有重要意义。
Abstract: Post-liver transplantation infection is the main obstacle affecting the long-term survival of recipients. Recent studies have found that immunosenescence-characterized by inflammatory senescence driven by senescence-associated secretory phenotype (SASP), myeloid shift, and intestinal flora imbalance is a key factor determining the susceptibility to postoperative infection and the prognosis of the graft. In liver transplant recipients, this process is exacerbated by donor liver age, ischemia-reperfusion injury, and long-term immunosuppression, manifested as delayed reconstitution of CD4+T cells and NK cells, reduced T cell receptor diversity, and metabolic remodeling. Clinical studies have confirmed that the immunosenescent state is significantly associated with multi-drug resistant bacterial infections, reactivation of latent viruses, and the risk of severe sepsis. Inflammatory markers such as serum IL-6 and TNF-α can be used as independent indicators for predicting the severity of infection and survival rate. Targeted elimination of senescent cells, regulation of the intestinal microbiome, blocking specific inflammatory pathways, and optimizing immunological strategies are expected to restore the immune homeostasis of recipients. Integrating immunosenescent markers into the clinical risk assessment system is of great significance for achieving individualized infection prevention and control after liver transplantation.
文章引用:陈伦伟, 吴传新. 免疫衰老与肝移植术后感染:从生物学机制到临床预后的深度评估[J]. 临床医学进展, 2026, 16(3): 1628-1635. https://doi.org/10.12677/acm.2026.163947

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