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ATP released by intestinal bacteria limits the generation of protective IgA against enteropathogens

Michele Proietti, Lisa Perruzza, Daniela Scribano, Giovanni Pellegrini, Rocco D’Antuono, Francesco Strati, Marco Raffaelli, Santiago F. Gonzalez, Marcus Thelen, Wolf-Dietrich Hardt, Emma Slack, Mauro Nicoletti and Fabio Grassi ()
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Michele Proietti: Università della Svizzera Italiana
Lisa Perruzza: Università della Svizzera Italiana
Daniela Scribano: University ‘‘Gabriele D’Annunzio’’, Via dei Vestini, Campus Universitario
Giovanni Pellegrini: University of Zurich
Rocco D’Antuono: Università della Svizzera Italiana
Francesco Strati: Università della Svizzera Italiana
Marco Raffaelli: Università della Svizzera Italiana
Santiago F. Gonzalez: Università della Svizzera Italiana
Marcus Thelen: Università della Svizzera Italiana
Wolf-Dietrich Hardt: Institute of Microbiology, ETH Zürich
Emma Slack: Institute of Microbiology, ETH Zürich
Mauro Nicoletti: University ‘‘Gabriele D’Annunzio’’, Via dei Vestini, Campus Universitario
Fabio Grassi: Università della Svizzera Italiana

Nature Communications, 2019, vol. 10, issue 1, 1-11

Abstract: Abstract T cell dependent secretory IgA (SIgA) generated in the Peyer’s patches (PPs) of the small intestine shapes a broadly diverse microbiota that is crucial for host physiology. The mutualistic co-evolution of host and microbes led to the relative tolerance of host’s immune system towards commensal microorganisms. The ATP-gated ionotropic P2X7 receptor limits T follicular helper (Tfh) cells expansion and germinal center (GC) reaction in the PPs. Here we show that transient depletion of intestinal ATP can dramatically improve high-affinity IgA response against both live and inactivated oral vaccines. Ectopic expression of Shigella flexneri periplasmic ATP-diphosphohydrolase (apyrase) abolishes ATP release by bacteria and improves the specific IgA response against live oral vaccines. Antibody responses primed in the absence of intestinal extracellular ATP (eATP) also provide superior protection from enteropathogenic infection. Thus, modulation of eATP in the small intestine can affect high-affinity IgA response against gut colonizing bacteria.

Date: 2019
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DOI: 10.1038/s41467-018-08156-z

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