To be, or not to be immunocompetent.

To be, or not to be immunocompetent.
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DOI:
10.1186/cc12897
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发表时间:
2013-09-13
期刊:
Critical care (London, England)
影响因子:
--
通讯作者:
Reinke P
Reinke P
中科院分区:
其他
文献类型:
--
作者:
Volk HD;Reinke P

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一些数据支持这样的观点,即炎症免疫应答受损是严重脓毒症的标志,恢复免疫活性的水平和时间对ICU患者的临床结局有重大影响。最近的研究表明,通过靶向负调控分子如CD 25、慢性T淋巴细胞活化抗原4和程序性死亡-1受体(PD-1)/PD-1 L来改善抗肿瘤免疫应答,为预防甚至逆转实验模型和患者中肿瘤生长的进展提供了新的机会。同样,严重脓毒症与这些负调控分子的表达增强有关,提示了一种逆转脓毒症免疫麻痹的新方法。因此,靶向脓毒症中的阴性分子可以逆转免疫麻痹并提高实验性脓毒症的存活率,正如Chang及其同事在最近一期的《危重病护理》中所示。这为克服适应性免疫应答的压倒性下调以预防脓毒症和/或改善脓毒症的恢复开辟了新的机会。
Several data support the view that impairment of the inflammatory-immune response is a hallmark of severe sepsis and the level and time of recovery to immunocompetence has a major impact on the clinical outcome of ICU patients. Recent studies demonstrate that improvement of anti-tumour immune response by targeting negative regulatory molecules, such as CD25, chronic T-lymphocyte activation antigen 4, and programmed death-1 receptor (PD-1)/PD-1 L, offers a novel opportunity to prevent or even reverse progression of tumour growth in experimental models and patients. Likewise, severe sepsis is associated with enhanced expression of those negative regulatory molecules, suggesting a novel approach to reverse immunoparalysis in sepsis. Consequently, targeting negative molecules in sepsis can reverse immunoparalysis and improve survival in experimental sepsis, as shown by Chang and colleagues in a recent issue of Critical Care. This opens new opportunities to overcome overwhelming downregulation of the adaptive immune response to prevent and/or improve recovery from sepsis.
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