A new mechanism for NK cell dysfunction.

On July 19th, Cell Metabolism, a journal of Cell Publishing Group, published online 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 National Research Center for Microscale Substances Science of the Chinese Academy of Sciences, and the research paper of The Board of The Natural Killer Cells by FBP1-Induced Progress And The Glycolyis.
NK cells are an effective lymphocyte that plays a vital role in the body's resistance to tumors.
NK cells do not need pre-sensitivity, i.e. they can directly kill tumor cells and promote the anti-tumor effect of adaptive immunity by secreting cytokines.
Based on the above principles, the value of NK cells in tumor immunotherapy has been widely recognized.
However, more and more studies have shown that during tumor growth, tumor cells can induce NK cell dysfunction through a variety of mechanisms to escape NK cell surveillance.
tumor development is a long process, including the initial period, the promoter period and the progression period of three stages.
and how NK cells interact with tumor cells throughout this process, it remains to be seen.
using the Kras mutation spontaneous lung cancer mouse model, the team proved that in the initial stage of tumor, NK cells have a strong anti-tumor function, can remove a large number of tumor cells, but in the tumor promotion period and progression, NK cells gradually lost anti-tumor ability. further research
found that NK cell loss of anti-tumor ability is closely related to its own metabolic disorders, when lung cancer occurred, tumor microenvironment accumulated a large number of conversion growth factor-b (TGF-beta), induced NK cells to increase the expression of fructose-1, 6-diphosformase (FBP1), abnormal expression of FBP1 inhibits the cell's own glycoenzyme metabolism, while destroying cell viability, eventually leading to cell dysfunction.
inhibits the activity of NK cell FBP1 and restores NK cell effect function, survival and in vivo tumor killing ability.
, FBP1 can weaken NK cell function by inhibiting THE metabolism of NK cell glycoenzyme, and targeting FBP1 to improve NK cell function can be used as a new strategy to optimize the immunotherapy of NK cell tumors.
research work has been supported by the National Natural Science Foundation of China and the Chinese Academy of Sciences' strategic leading science and technology special funding.
communications by Wei Haiming and Tian Zhigang, and the first author is Dr. Jing Jing.
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