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    T Follicular Helper Cells Promote a Beneficial Gut Ecosystem for Host Metabolic Homeostasis by Sensing Microbiota-Derived Extracellular ATP

    Access Status
    Open access via publisher
    Authors
    Perruzza, L.
    Gargari, G.
    Proietti, M.
    Fosso, B.
    D'Erchia, A.
    Faliti, C.
    Rezzonico-Jost, T.
    Scribano, D.
    Mauri, L.
    Colombo, D.
    Pellegrini, G.
    Moregola, A.
    Mooser, C.
    Pesole, G.
    Nicoletti, M.
    Norata, Giuseppe
    Geuking, M.
    McCoy, K.
    Guglielmetti, S.
    Grassi, F.
    Date
    2017
    Type
    Journal Article
    
    Metadata
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    Citation
    Perruzza, L. and Gargari, G. and Proietti, M. and Fosso, B. and D'Erchia, A. and Faliti, C. and Rezzonico-Jost, T. et al. 2017. T Follicular Helper Cells Promote a Beneficial Gut Ecosystem for Host Metabolic Homeostasis by Sensing Microbiota-Derived Extracellular ATP. Cell Reports. 18 (11): pp. 2566-2575.
    Source Title
    Cell Reports
    DOI
    10.1016/j.celrep.2017.02.061
    ISSN
    2211-1247
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/56397
    Collection
    • Curtin Research Publications
    Abstract

    © 2017 The Authors The ATP-gated ionotropic P2X7 receptor regulates T follicular helper (Tfh) cell abundance in the Peyer's patches (PPs) of the small intestine; deletion of P2rx7, encoding for P2X7, in Tfh cells results in enhanced IgA secretion and binding to commensal bacteria. Here, we show that Tfh cell activity is important for generating a diverse bacterial community in the gut and that sensing of microbiota-derived extracellular ATP via P2X7 promotes the generation of a proficient gut ecosystem for metabolic homeostasis. The results of this study indicate that Tfh cells play a role in host-microbiota mutualism beyond protecting the intestinal mucosa by induction of affinity-matured IgA and suggest that extracellular ATP constitutes an inter-kingdom signaling molecule important for selecting a beneficial microbial community for the host via P2X7-mediated regulation of B cell help.

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