Liver myofibroblasts from hepatitis B related liver failure patients may regulate natural killer cell function via PGE2
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  • 作者:Min Zhang (1)
    Fenglan Wang (2) (3)
    Yutian Chong (1)
    Qiang Tai (4)
    Qiyi Zhao (1)
    Yubao Zheng (1)
    Liang Peng (1)
    Shumei Lin (2)
    Zhiliang Gao (1)

    1. Department of Infectious Diseases
    ; Third Affiliated Hospital of Sun Yat-sen University ; No. 600 Tianhe Road ; Guangzhou ; 510630 ; Guangdong Province ; China
    2. Department of Infectious Diseases
    ; First Affiliated Hospital of Medical College of Xi鈥瞐n Jiaotong University ; No. 277 Yanta West Road ; Xi鈥瞐n ; 710061 ; Shanxi Province ; China
    3. Department of Infectious Diseases
    ; the Eighth Hospital of Xi鈥瞐n ; Xi鈥瞐n ; China
    4. Department of Hepatic Surgury
    ; First Affiliated Hospital of Sun Yat-sen University ; Guangzhou ; China
  • 关键词:Liver myofibroblasts ; Natural killer cell ; Immune ; mediated liver injury ; Liver failure ; Hepatitis B
  • 刊名:Journal of Translational Medicine
  • 出版年:2014
  • 出版时间:December 2014
  • 年:2014
  • 卷:12
  • 期:1
  • 全文大小:2,782 KB
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  • 刊物主题:Biomedicine general; Medicine/Public Health, general;
  • 出版者:BioMed Central
  • ISSN:1479-5876
文摘
Background Natural killer (NK) cells are abundant in the liver and constitute a major innate immune component that contributes to immune-mediated liver injury. However, few studies have investigated the phenotypes and functions of NK cells involved in hepatitis B related liver failure (LF), and the precise mechanism underlying NK cell regulation is not fully understood. Methods We detected the percentage and function of peripheral NK cells both in hepatitis B related LF patients and healthy volunteers by flow cytometry and isolated the liver myofibroblasts (LMFs) from hepatitis B related LF livers. To determine the possible effects of LMFs on NK cells, mixed cell cultures were established in vitro. Results We found a down-regulated percentage of peripheral NK cells in hepatitis B related LF patients, and their NK cells also displayed decreased activated natural cytotoxicity receptors (NCRs) and cytokine production. In a co-culture model, LMFs sharply attenuated IL-2-induced NK cell triggering receptors, cytotoxicity, and cytokine production. The inhibitory effect of LMFs on NK cells correlated with their ability to produce prostaglandin (PG) E2. Conclusion These data suggest that LMFs may protect against immune-mediated liver injury in hepatitis B related LF patients by inhibiting NK cell function via PGE2.

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