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首页> 外文期刊>Infection and immunity >Natural killer cell activation and interferon production by peripheral blood lymphocytes after exposure to bacteria.
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Natural killer cell activation and interferon production by peripheral blood lymphocytes after exposure to bacteria.

机译:暴露于细菌后,外周血淋巴细胞自然杀伤细胞活化并产生干扰素。

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We have previously shown that peripheral blood natural killer (NK) cells have significant levels of cytotoxic activity against Shigella flexneri-infected HeLa cells. In this report, we show that NK cell activity against K562 tumor cells and Shigella flexneri-infected HeLa cells can be greatly enhanced by preincubating peripheral blood lymphocytes (PBL) for 18 h with kanamycin-treated Shigella flexneri or Salmonella typhimurium. Cell-free supernatants obtained from PBL-bacteria cultures contained high levels of interferon (IFN) activity, which was characterized as a mixture of IFN-gamma and IFN-alpha. Cytotoxic activity associated with PBL precultured with shigellae was associated with predominantly CD16+ (Leu-11+) and CD2+ (OKT-11+) cells. Further, IFN production was dependent upon the presence of CD16+ and CD2+ cells at culture initiation. Enhancement of cytotoxic activity associated with PBL-bacteria cultures did not, however, appear to be dependent upon IFN production, since low numbers of bacteria which failed to stimulate IFN production induced high levels of NK cell activity. Lipopolysaccharide appeared not to be involved in bacteria-induced IFN production or enhanced NK cell activity, since Salmonella lipopolysaccharide failed to induce IFN production or enhance NK cell activity. These results suggest that IFN production by NK cells and the killing of bacteria-infected cells play an important role in host defense against facultative intracellular bacterial infections.
机译:先前我们已经表明,外周血自然杀伤(NK)细胞对弗氏志贺氏菌感染的HeLa细胞具有显着水平的细胞毒活性。在本报告中,我们表明,通过与卡那霉素治疗的志贺氏菌或鼠伤寒沙门氏菌预孵育外周血淋巴细胞(PBL)18 h,可以大大增强针对K562肿瘤细胞和志贺氏菌感染的HeLa细胞的NK细胞活性。从PBL细菌培养物中获得的无细胞上清液含有高水平的干扰素(IFN)活性,其特征是IFN-γ和IFN-α的混合物。与志贺杆菌预培养的PBL相关的细胞毒活性主要与CD16 +(Leu-11 +)和CD2 +(OKT-11 +)细胞有关。此外,IFN产生取决于培养开始时CD16 +和CD2 +细胞的存在。然而,与PBL细菌培养有关的细胞毒性活性的增强似乎并不依赖于IFN的产生,因为未能刺激IFN产生的细菌数量少,诱导了高水平的NK细胞活性。脂多糖似乎不参与细菌诱导的IFN产生或增强的NK细胞活性,因为沙门氏菌脂多糖无法诱导IFN产生或增强NK细胞活性。这些结果表明,NK细胞产生的IFN和杀死细菌感染的细胞在宿主抵抗兼性细胞内细菌感染的防御中起着重要作用。

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