败血症的免疫学特征包括炎症介导的细胞因子风暴、凋亡驱动的淋巴细胞减少以及长期的免疫失调。虽然早期的临床工作集中在通过第一阶段增加患者的生存率，但现在的研究正转向关注败血症对幸存者免疫健康的长期影响。特别是，最重要的任务是解析免疫系统如何被抑制，从而导致二次感染的发病率增加。在本综述中，我们介绍了先天（自然杀伤细胞、树突状细胞）和适应性（T细胞、B细胞）免疫细胞中的数量变化和功能重编程对小鼠和人宿主中慢性免疫失调的贡献。我们简要讨论了小鼠模型中的免疫学经验如何影响败血症严重程度、免疫功能障碍和临床相关性。最后，我们深入探讨自身免疫和癌症等共病如何影响宿主对败血症的易感性以及相关的免疫功能障碍。 版权所有©2023年美国免疫学家协会。

The immunological hallmarks of sepsis include the inflammation-mediated cytokine storm, apoptosis-driven lymphopenia, and prolonged immunoparalysis. Although early clinical efforts were focused on increasing the survival of patients through the first phase, studies are now shifting attention to the long-term effects of sepsis on immune fitness in survivors. In particular, the most pertinent task is deciphering how the immune system becomes suppressed, leading to increased incidence of secondary infections. In this review, we introduce the contribution of numerical changes and functional reprogramming within innate (NK cells, dendritic cells) and adaptive (T cells, B cells) immune cells on the chronic immune dysregulation in the septic murine and human host. We briefly discuss how prior immunological experience in murine models impacts sepsis severity, immune dysfunction, and clinical relevance. Finally, we dive into how comorbidities, specifically autoimmunity and cancer, can influence host susceptibility to sepsis and the associated immune dysfunction.Copyright © 2023 by The American Association of Immunologists, Inc.