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    Home > Biochemistry News > Biotechnology News > The liver resides in NK cells that can negatively adjust the antiviral immune response of T cells and its mechanism.

    The liver resides in NK cells that can negatively adjust the antiviral immune response of T cells and its mechanism.

    • Last Update: 2020-08-05
    • Source: Internet
    • Author: User
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    Recently, Cell Publishing Group's journal Ofimmunity published the research paper "Liver-resident NK cells control anti-campaign of hepatic T cells via PD-1/PD-L1 axis" by the Department of Life Sciences and Medicine of the Chinese University of Science and Technology, the Key Laboratory of Natural Immunology and Chronic Diseases of the Chinese Academy of Sciences, and the Tian Zhigang Group of the National Research Center for Microscale Matterscience.
    the liver has unique immune tolerance properties, is the main place where many viruses replicate in the body, liver T cells often do not produce an effective immune response to remove the virus, resulting in persistent infection of the virus.
    However, the regulatory mechanism of low antiviral capacity of liver T cells is not very clear.
    Tian Zhigang's team first reported the presence of a unique resident NK (River-resident NK, LrNK) cells (J Clin Invest 123,1444-1456 (2013)) in the liver of adult mice in 2013.
    the liver this special lrNK cells and peripheral circulation of classical NK (cNK) cells, not only the episotype development differentiation regulatory mechanism is different, but also the expression of the effect molecules are also different.
    transcriptional histology results suggest that LrNK cells express immune negative sinnial and tolerance-inducing genes relative to cNK cells.
    Given that the liver's immune tolerance characteristics are closely related to the poor response of T cells, whether LrNK cells can maintain liver immunity by regulating the T-cell response is an important starting point for the study.
    team used lrNK cell defect mice to conduct experiments and found that after the virus infection of the defective mice, T-cell function was enhanced and viral titer decreased in the liver of mice.
    to the external transfer of LrNK cells in normal mice or LrNK cell defects can inhibit the response of antiviral T cells in the liver, while cNK cells promote T-cell response.
    further inviviable and out-of-body experiments found that LrNK cells rely on PD-L1 on their surface to perform functional inhibition of T cells in the liver.
    this paper systematically explains the complete opposite function of LrNK and cNK cells in regulating T-cell response, suggesting that LrNK cells play an important role in the maintenance of the liver's immune tolerance microenvironment.
    this work provides a new basis for understanding the intrinsic relationship between NK cell subgroup composition and regional immune characteristics shaping.
    the research work is funded by the NSFC and the Chinese Academy of Sciences.
    communication is written by Tian Zhigang, a professor at the University of Science and Technology of China, and Peng Hui, an associate professor, and the first author is Zhou Jing, Ph.D., China University of Science and Technology.
    related research progress reveals the molecular mechanism of EGFR/ERK signaling pathway seisciating liver cancer cell resistance, Liu Yang, a researcher in the Disease Genomics Research Group (1832 Group) of the Center for Translational Medicine Science Research Center of the Research Department of the Dalian Institute of Chemical Physics of the Chinese Academy of Sciences, has made new progress in the field of tumor translational medicine.
    related findings were published in the Journal of Experimental and Clinical Cancer Research (J Exp Clin Cancer Res).
    currently, sorafenib and lenvatinib are FDA-approved targeted drugs for first-line treatment of liver cancer, but these drugs are less responsive in the treatment of liver cancer and generally only extend the patient's survival for about 3 months.
    past studies have shown that BRD4 (BET-Bromodomain4) inhibitor, JQ1, which can cause apoptosis in liver cancer by inhibiting c-Myc transcription and expression, has important potential in the clinical treatment of liver cancer.
    , however, only some of the highly expressed liver cancer cells of c-Myc are sensitive to JQ1, and the molecular mechanism is not clear.
    to address this issue, the team used genomics research methods to find new acquired EGFR-I645L mutations in JQ1 insensitive liver cancer cell lines.
    the mutation continuously activates the MAPK signaling pathway to promote phosphorylation at the c-Myc protein ser 62-bit site, thereby stabilizing c-Myc and mediasetting tumor cell resistance to JQ1.
    studies have also found that inviviable and in vitro combinations of JQ1 and EGFR or ERK specific inhibitors can effectively inhibit tumor cell growth.
    the results of the study illustrate the molecular mechanism of hepatic cancer cells resistance to JQ1, and provide a theoretical basis for improving the effectiveness of clinical anti-tumor drugs.
    and above research work has been funded by the National Key Research and Development Program, the National Natural Science Foundation of China, the Dalian Chemical Innovation Fund, and the "100-person Plan" of the Chinese Academy of Sciences.
    Source: China University of Science and Technology/Dalian Institute of Chemical Physics.
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