干扰素- α诱导的自然杀伤细胞改变与丙型肝炎感染患者的治疗结果相关。

Hepatitis research and treatment Pub Date : 2013-01-01 Epub Date: 2013-08-13 DOI:10.1155/2013/374196
Shinji Shimoda, Kosuke Sumida, Sho Iwasaka, Satomi Hisamoto, Hironori Tanimoto, Hideyuki Nomura, Kazufumi Dohmen, Kazuhiro Takahashi, Akira Kawano, Eiichi Ogawa, Norihiro Furusyo, Koichi Akashi, Jun Hayashi
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引用次数: 2

摘要

的目标。我们分析了预处理自然杀伤(NK)细胞功能,目的是预测持续病毒学反应(SVR)或与治疗反应密切相关的白细胞介素(IL) 28B多态性。方法。用toll样受体(TLR) 4配体和IFN- α激活HCV基因型1和病毒滴度高的慢性肝炎患者外周血NK细胞。使用流式细胞术分析评估细胞表面标记物,使用酶联免疫吸附试验(ELISA)评估IFN- γ的产生。对每位患者采集的DNA进行19号染色体上IL28B基因区(rs8099917)多态性的基因分型。结果。与无应答(NR)患者相比,SVR患者的IFN- γ的产生明显更高,而SVR患者和NR患者的细胞表面标志物相似。与IFN- γ产生相关的IL28B基因型分布无显著差异。结论。在SVR患者和NR患者之间观察到NK细胞功能的差异,提示NK细胞在独立于IL28B基因型的治疗反应中发挥潜在作用。
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Interferon- α -Induced Changes to Natural Killer Cells Are Associated with the Treatment Outcomes in Patients with HCV Infections.

Aim. We analyzed the pretreatment natural killer (NK) cell functions with the aim of predicting the sustained virological response (SVR) or the interleukin (IL) 28B polymorphism that is strongly associated with the treatment response. Methods. The peripheral NK cells from chronic hepatitis patients with HCV genotype 1 and high virus titers were activated using a Toll-like receptor (TLR) 4 ligand and IFN- α . The cell surface markers were evaluated using a flow cytometric analysis, and IFN- γ production was evaluated using an enzyme-linked immunosorbent assay (ELISA). The genotyping of the polymorphisms in the IL28B gene region (rs8099917) on chromosome 19 was performed on the DNA collected from each patient. Results. The production of IFN- γ was significantly higher in the SVR patients compared with the no-response (NR) patients, whereas the cell surface markers were similar between the SVR and the NR patients. There were no significant differences found in the IL28B genotype distribution associated with the production of IFN- γ . Conclusion. Differences in the NK cell functions were observed between the SVR patients and the NR patients, suggesting that NK cells play a potential role in the treatment response independent of the IL28B genotype.

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