免疫细胞在移植肾冷缺血再灌注损伤中的研究进展

Research progress on immune cells in cold ischemia-reperfusion injury of renal allografts

摘要

移植肾冷缺血再灌注损伤（CIRI）是导致移植肾功能延迟恢复和远期失功的重要原因，其发生发展涉及能量代谢障碍、氧化应激增强及无菌性炎症反应等多重机制。近年来研究表明，免疫细胞在CIRI过程中发挥核心调控作用。冷缺血及再灌注过程中释放的损伤相关分子模式可激活先天免疫，促使中性粒细胞、巨噬细胞和树突状细胞等迅速募集并放大炎症反应；同时，适应性免疫细胞如T细胞和B细胞被进一步激活，参与炎症持续、免疫耐受破坏及移植物损伤的进展。不同免疫细胞亚群之间通过细胞因子、趋化因子及抗原呈递等方式形成复杂的相互作用网络，共同决定CIRI的严重程度及结局。本文系统综述了先天免疫与适应性免疫细胞在移植肾CIRI中的作用机制及其相互关联，并总结了靶向免疫细胞的潜在干预策略，旨在为改善肾移植临床预后提供理论依据。

Abstract

Cold ischemia-reperfusion injury (CIRI) is a major contributor to delayed graft function and long-term graft failure after kidney transplantation. Its pathogenesis involves multiple mechanisms, including energy metabolism disorders, oxidative stress and sterile inflammatory responses. Increasing evidence indicates that immune cells play a central regulatory role in the initiation and progression of CIRI. Damage-associated molecular patterns released during cold ischemia and reperfusion activate innate immunity, leading to the rapid recruitment of neutrophils, macrophages, dendritic cells and amplification of inflammatory cascades. Subsequently, adaptive immune cells, including T cells and B cells, are activated and further contribute to sustained inflammation, disruption of immune tolerance and graft injury. Through cytokine signaling, chemokine-mediated recruitment and antigen presentation, different immune cell subsets form a complex interactive network that ultimately determines the severity and outcome of CIRI. This review summarizes the roles and mechanisms of innate and adaptive immune cells in renal allograft CIRI, highlights their interconnections, and discusses emerging immune cell-targeted therapeutic strategies, aiming to provide a theoretical basis for improving clinical outcomes in kidney transplantation.

关键词

移植肾 / 冷缺血再灌注损伤 / 免疫细胞 / 细胞免疫治疗

Key words

transplanted kidney / cold ischemia-reperfusion injury / immune cells / cellular immunotherapy

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基金资助

国家自然科学基金面上项目(82270817)