Centre for Inflammatory Diseases, School of Clinical Sciences, Monash University and Monash Infectious Diseases, Monash Health, Australia.
Centre for Inflammatory Diseases, School of Clinical Sciences, Monash University, Australia; Department of Nephrology, Monash Medical Centre, Clayton, Victoria 3168, Australia.
Transplant Rev (Orlando). 2019 Apr;33(2):87-98. doi: 10.1016/j.trre.2018.10.001. Epub 2018 Oct 9.
Despite improvements in graft survival, solid organ transplantation is still associated with considerable infection induced morbidity and mortality. If we were able to show that serious infection risk was associated with excessive suppression of immune capacity, we would be justified in "personalizing" the extent of immunosuppression by carefully monitored reduction to see if we can improve immune compromize without increasing the risk of rejection. Reliable biomarkers are needed to identify this patients at an increased risk of infection. This review focuses on the currently available evidence in solid organ transplant recipients for immune non-pathogen specific biomarkers to predict severe infections with the susceptibility to particular pathogens according to the component of the immune system that is suppressed. This review is categorized into immune biomarkers representative of the humoral, cellular, phagocytic, natural killer cell and complement system. Biomarkers humoral and cellular systems of the that have demonstrated an association with infections include immunoglobulins, lymphocyte number, lymphocyte subsets, intracellular concentrations of adenosine triphosphate in stimulated CD4 cells and soluble CD30. Biomarkers of the innate immune system that have demonstrated an association with infections include natural killer cell numbers, complement and mannose binding lectin. Emerging evidence shows that quantification of viral nucleic acid (such as Epstein Barr Virus) can act as a biomarker to predict all-cause infections. Studies that show the most promise are those in which several immune biomarkers are assessed in combination. Ongoing research is required to validate non-pathogen specific immune biomarkers in multi-centre studies using standardized study designs.
尽管移植物存活率有所提高,但实体器官移植仍与相当大的感染相关发病率和死亡率有关。如果我们能够证明严重感染风险与免疫能力过度抑制有关,我们就有理由通过仔细监测减少免疫抑制的程度来“个性化”免疫抑制的程度,以观察我们是否可以在不增加排斥风险的情况下改善免疫抑制。需要可靠的生物标志物来识别感染风险增加的患者。这篇综述重点介绍了目前在实体器官移植受者中用于免疫非病原体特异性生物标志物的证据,以根据被抑制的免疫系统成分预测具有特定病原体易感性的严重感染。这篇综述分为代表体液、细胞、吞噬细胞、自然杀伤细胞和补体系统的免疫生物标志物。已证明与感染相关的体液和细胞系统免疫生物标志物包括免疫球蛋白、淋巴细胞数量、淋巴细胞亚群、刺激 CD4 细胞中三磷酸腺苷的细胞内浓度和可溶性 CD30。已证明与感染相关的固有免疫系统生物标志物包括自然杀伤细胞数量、补体和甘露糖结合凝集素。新出现的证据表明,定量检测病毒核酸(如 Epstein Barr 病毒)可以作为预测所有原因感染的生物标志物。最有希望的研究是那些评估几种免疫生物标志物组合的研究。需要进行正在进行的研究,以使用标准化研究设计在多中心研究中验证非病原体特异性免疫生物标志物。