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    Home > Active Ingredient News > Immunology News > ​Science 'trained' memory cells in mouse gut

    ​Science 'trained' memory cells in mouse gut

    • Last Update: 2022-06-19
    • Source: Internet
    • Author: User
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    AuthorNovember In the immune system, there is a group of cells that have a "memory" of invasion from the outside world and can prepare for the re-invasion of the same bacteria and viruses.
    This group of lymphocytes is called memory cells
    .

    (Yes, the editor recommends the animation "Working Cells" to everyone again.
    CCTV Six Princesses can even watch the Chinese version.
    Good popular science is worth pushing again and again.
    For example, it is strongly recommended that you continue to pay attention to BioArt :D)
    .

    Memory cells - "Working cells" There is such a group of cells in lymphocytes called ILC3s (Group 3 innate lymphoid cells), which have innate immune effects and contribute to the host's defense
    .

    But it is unknown how this population of cells can be stably modified in contact with pathogens to have a "memory" of the pathogen
    .

    To this end, the research group of James P.
    Di Santo of the Pasteur Institute in Paris, France, published a paper entitled Trained ILC3 responses promote intestinal defense in Science, and found that mice were continuously activated after exposure to Citrobacter rodentium.
    When the pathogen comes again, these "trained" ILC3s will proliferate in large numbers and will promote and enhance the interleukin IL-22 response, indicating that the ILC3s lymphocyte population has a memory for the pathogen, and at the same time in this work.
    The findings also contribute to the understanding of processes such as gut immunity
    .

    Special immune cell populations can promote and maintain the function of the intestinal barrier, and maintain tolerance to various microorganisms on the surface of the intestinal mucosa, including effector T cells and memory T cells, providing long-term immune monitoring for the body
    .

    ILC3s are highly enriched in the gut and coordinate the development of lymphoid tissue and the defense of the intestinal mucosa [1-2]
    .

    ILC3s are indirectly activated by soluble factors derived from epithelial and hematopoietic sentinel cells after infection, and then secrete interleukins IL-17 and IL-22 to protect the host [3-5]
    .

    But whether ILC3s cells have any degree of long-term adaptation to pathogens to help the body improve immune function is unknown
    .

    To do this, the authors infected the mouse gut with Citrobacter murines, a pathogen that can cause colitis similar to infection with human enteropathogens
    .

    The authors found that when mice were re-infected with Citrobacter murines, the number of ILC3s increased significantly and rapidly while other cell types were stable
    .

    The absolute amount and increasing frequency of IL-22 were similar to ILC3 cells, but the T cells that also expressed IL-22 were basically unchanged
    .

    Because this population of cells is highly functional and persistent, the authors refer to this population as "trained" ILC3 cells ("trained ILC3s", Tr-ILC3s) (Figure 1)
    .

    Figure 1 "Trained" ILC3 cells in the mouse gut This group of trained Tr-ILC3s memory cells helps mice to produce IL-22 in the face of re-invasion of pathogens, which is the result of naïve ILC3 cells no ability
    .

    Further, the authors wondered whether this "memory" was absolutely specific, thus replacing another pathogen during reinfection, and found that infection with another pathogen could also trigger interleukin ILC3 activation and IL- 22, and therefore, the immune memory of this population of Tr-ILC3s memory cells lacks antigen specificity
    .

    The authors then performed RNA-seq sequencing analysis of Tr-ILC3s memory cells as well as naïve ILC3 cells, and found that after infection in mice, ILC3 memory cells showed changes from glycolysis to the Krebs cycle, oxidative phosphorylation, fatty acid synthesis and Metabolic shifts such as oxidation-related gene expression, in addition to higher oxygen consumption rates in ILC3 memory cells, suggest increased mitochondrial fitness in this population of cells
    .

    Collectively, this work identified a population of trained immune memory cells, Tr-ILC3s, in the mouse gut, which proliferated and rapidly produced IL-22 when re-encountered by pathogens after initial pathogen infection, thereby promoting mucosal defense
    .

    This population of Tr-ILC3 memory cells may provide new reference ideas for the prevention or treatment of diseases caused by inflammation or pathogen invasion of the barrier surface
    .

    Original link: https:// Publisher: Eleven References 1.
    Hooper LV, Macpherson AJ.
    Immune adaptations that maintain homeostasis with the intestinal microbiota.
    Nat Rev Immunol.
    2010 ;10(3):159-169.
    doi:10.
    1038/nri27102.
    Spits H, Artis D, Colonna M, et al.
    Innate lymphoid cells--a proposal for uniform nomenclature.
    Nat Rev Immunol.
    2013;13(2): 145-149.
    doi:10.
    1038/nri33653.
    Satoh-Takayama N, Vosshenrich CA, Lesjean-Pottier S, et al.
    Microbial flora drives interleukin 22 production in intestinal NKp46+ cells that provide innate mucosal immune defense.
    Immunity.
    2008;29(6 ): 958-970.
    doi: 10.
    1016/j.
    immuni.
    2008.
    11.
    0014.
    Buonocore S, Ahern PP, Uhlig HH, et al.
    Innate lymphoid cells drive interleukin-23-dependent innate intestinal pathology.
    Nature.
    2010;464(7293 ): 1371-1375.
    doi: 10.
    1038/nature089495.
    Cella M, Fuchs A, Vermi W, et al.
    A human natural killer cell subset provides an innate source of IL-22 for mucosal immunity.
    Nature.
    2009;457(7230):722-725.
    doi:10.
    1038/nature07537 Notes for reprinting【Original article】BioArt original article, welcome to forward and share , reprinting is prohibited without permission, and the copyright of all works published is owned by BioArt
    .

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    .


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