T-cell-mediated immunity and the role of TRAIL in sepsis-induced immunosuppression.

T-cell-mediated immunity and the role of TRAIL in sepsis-induced immunosuppression.
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DOI:
10.1615/critrevimmunol.2013006721
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发表时间:
2013
影响因子:
1.3
通讯作者:
Griffith TS
Griffith TS
中科院分区:
医学4区
文献类型:
--
作者:
Condotta SA;Cabrera-Perez J;Badovinac VP;Griffith TS

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脓毒症是大多数重症监护病房死亡的主要原因,脓毒症患者的死亡通常不是由最初的脓毒症事件引起的,而是由随后的医院感染引起的。严重败血症存活下来的患者通常表现出严重的免疫功能受损。在败血症期间,不仅淋巴细胞和髓细胞显著凋亡,耗尽免疫系统的关键成分,而且剩余免疫细胞的功能也下降。动物和人类的研究表明,败血症期间发生的免疫缺陷可能对其发病机制和随后的死亡率至关重要。这篇综述的重点是脓毒症诱导的CD8 t细胞区室的改变,它可以影响继发性异源感染的控制。了解脓毒症事件如何通过凋亡死亡和稳态增殖直接影响CD8 t细胞群,以及通过免疫介导的抑制间接影响CD8 t细胞群,将为开发新的治疗方案提供有价值的起点。
Sepsis is the leading cause of death in most intensive care units, and the death of septic patients usually does not result from the initial septic event but rather from subsequent nosocomial infections. Patients who survive severe sepsis often display severely compromised immune function. Not only is there significant apoptosis of lymphoid and myeloid cells that depletes critical components of the immune system during sepsis, there is also decreased function of the remaining immune cells. Studies in animals and humans suggest the immune defects that occur during sepsis may be critical to the pathogenesis and subsequent mortality. This review is focused on sepsis-induced alterations with the CD8 T-cell compartment that can affect the control of secondary heterologous infections. Understanding how a septic event directly influences CD8 T-cell populations through apoptotic death and homeostatic proliferation and indirectly by immune-mediated suppression will provide valuable starting points for developing new treatment options.
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