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Role of IL-12 in overcoming the low responsiveness of NK cells to missing self after traumatic brain injury

机译:IL-12在创伤性脑损伤后克服NK细胞对缺失自身的低响应性的作用

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摘要

Blood samples from 32 patients with severe Traumatic brain injury (TBI) were studied and compared with 11 cardiac surgery patients, and 29 healthy controls. A dramatic decreased expression of HLA class I molecules on monocytes was associated with increased KIR+ NK cell frequency in TBI patients. Overall, the phenotype of TBI NK cells marked by KIR and CD57 expression and lower level of NKp46 and DNAM-1 reflected a differentiated state. The NK-cell response to missing self was marked by lower degranulation and lower IFN-gamma production after stimulation with HLA class I deficient cell line. In contrast, the NK-cell ADCC was not altered. IL-12 was able to restore both IFN-gamma production and the cytotoxicity capacities of NM cells. This study provides the first extensive description of the phenotype and functions of NM cells in TBI patients. Further evaluation of IL-12 treatment to overcome immunosuppression-induced nosocomial infections is warranted. (C) 2015 Elsevier Inc. All rights reserved.
机译:研究了来自32例严重创伤性脑损伤(TBI)患者的血液样本,并与11例心脏手术患者和29例健康对照组进行比较。 HLA I类分子对单核细胞分子的显着降低与TBI患者中的KIR + NK细胞频率增加有关。总之,由KIR和CD57表达标记的TBI NK细胞的表型和低水平的NKP46和DNAM-1反映了差异化状态。在用HLA类I缺陷细胞系刺激后,对缺失自身的NK细胞反应标记为较低的脱粒和较低的IFN-Gamma生产。相反,NK-Cell ADCC未被改变。 IL-12能够恢复IFN-Gamma生产和NM细胞的细胞毒性容量。该研究提供了TBI患者在NM细胞的表型和功能的第一种广泛描述。有必要进一步评价IL-12治疗以克服免疫抑制诱导的神经感染。 (c)2015 Elsevier Inc.保留所有权利。

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