Thaunat Olivier, Lakkis Fadi G, Kosmoliaptsis Vasilis, Schinstock Carrie, Tambur Anat, Heidt Sebastiaan, Naesens Maarten
Lyon-Est Medical Faculty, Claude Bernard University, Lyon, France; Department of Internal Medicine, Hospices Civils de Lyon, Edouard Herriot Hospital, Lyon, France; Centre International de Recherche en Infectiologie, INSERM U1111, Université Claude Bernard Lyon I, Centre National de la Recherche Scientifique UMR5308, Ecole Normale Supérieure de Lyon, Lyon, France.
Departments of Surgery, Immunology, and Medicine, Thomas E. Starzl Transplantation Institute, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Am J Transplant. 2025 Jul 5. doi: 10.1016/j.ajt.2025.06.030.
In solid organ transplantation, the alloimmune response is traditionally attributed to the action of alloreactive T cells that recognize mismatched human leukocyte antigens, as well as antibody formation and antibody-mediated rejection. However, recent evidence indicates that these paradigms of involvement of the adaptive immune system in organ transplant rejection do not explain all cases of graft inflammation and that innate cell allorecognition plays a role. This review, conducted by the innate team of the Sensitization in Transplantation Assessment of Risk workgroup, summarizes the concepts and empirical evidence supporting innate allorecognition. The focus is on natural killer cell activation via missing self and monocyte activation through the signal regulatory protein α-CD47 pathway and SIRPα gene polymorphisms. A consensus definition of genetic missing self is proposed, necessitating both donor and recipient human leukocyte antigen class I genotyping and evaluation of the recipient inhibitory killer-cell immunoglobulin-like receptor genotype. Although in vitro studies and preclinical validations corroborate the potential of innate allorecognition concepts, further research is required to establish clinical utility. This article delineated future research directions to bridge the gap between theoretical promise and practical application in clinical transplantation.
在实体器官移植中,传统上同种免疫反应被认为是由识别不匹配人类白细胞抗原的同种反应性T细胞的作用,以及抗体形成和抗体介导的排斥反应所导致的。然而,最近的证据表明,适应性免疫系统参与器官移植排斥反应的这些模式并不能解释所有的移植物炎症病例,并且天然细胞同种识别也发挥了作用。这篇由移植致敏风险评估工作组的天然免疫团队撰写的综述,总结了支持天然同种识别的概念和实验证据。重点是通过“自我缺失”激活自然杀伤细胞,以及通过信号调节蛋白α-CD47途径和信号调节蛋白α(SIRPα)基因多态性激活单核细胞。本文提出了基因“自我缺失”的共识定义,这需要对供体和受体的人类白细胞抗原I类进行基因分型,并评估受体抑制性杀伤细胞免疫球蛋白样受体的基因型。尽管体外研究和临床前验证证实了天然同种识别概念的潜力,但仍需要进一步研究以确定其临床应用价值。本文阐述了未来的研究方向,以弥合临床移植中理论前景与实际应用之间的差距。