Gao Xun, Cai Shijie, Li Xiao, Wu Guoqiu
Center of Clinical Laboratory Medicine, Zhongda Hospital, Southeast University, Nanjing, Jiangsu, China.
Department of Laboratory Medicine, Medical School of Southeast University, Nanjing, Jiangsu, China.
Front Immunol. 2025 Apr 29;16:1577105. doi: 10.3389/fimmu.2025.1577105. eCollection 2025.
Sepsis, a life-threatening organ dysfunction resulting from a dysregulated host response to infection, initiates a complex immune response that varies over time, characterized by sustained excessive inflammation and immunosuppression. Sepsis-induced immunosuppression is now recognized as a major cause of septic death, and identifying effective strategies to counteract it poses a significant challenge. This immunosuppression results from the disruption of immune homeostasis, characterized by the abnormal death of immune effector cells, hyperproliferation of immune suppressor cells, release of anti-inflammatory cytokines, and expression of immune checkpoints. Preclinical studies targeting immunosuppression, particularly with immune checkpoint inhibitors, have shown promise in reversing immunocyte dysfunctions and establishing host resistance to pathogens. Here, our review highlights the mechanisms of sepsis-induced immunosuppression and current diagnostic biomarkers, as well as immune-enhancing strategies evaluated in septic patients and therapeutics under investigation.
脓毒症是宿主对感染的失调反应导致的危及生命的器官功能障碍,它引发了一种随时间变化的复杂免疫反应,其特征是持续的过度炎症和免疫抑制。脓毒症诱导的免疫抑制现在被认为是脓毒症死亡的主要原因,确定有效的应对策略面临重大挑战。这种免疫抑制是由免疫稳态的破坏引起的,其特征是免疫效应细胞的异常死亡、免疫抑制细胞的过度增殖、抗炎细胞因子的释放以及免疫检查点的表达。针对免疫抑制的临床前研究,特别是使用免疫检查点抑制剂的研究,在逆转免疫细胞功能障碍和建立宿主对病原体的抵抗力方面显示出了前景。在这里,我们的综述强调了脓毒症诱导的免疫抑制机制和当前的诊断生物标志物,以及在脓毒症患者中评估的免疫增强策略和正在研究的治疗方法。