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Microbiome-derived inosine modulates response to checkpoint inhibitor immunotherapy
Lukas Franz Mager (University of Calgary), Regula Burkhard (University of Calgary), Nicola Pett (University of Calgary), Noah C.A. Cooke (University of Calgary), Kirsty Brown (University of Calgary), Hena R. Ramay (University of Calgary), Seungil Paik (University of Calgary, Alberta Children's Hospital Research Institute), John Stagg (Centre Hospitalier de l’Université de Montréal, Institut du cancer de Montréal), Ryan A. Groves (University of Calgary), Marco Gallo (University of Calgary, Alberta Children's Hospital Research Institute), Ian A. Lewis (University of Calgary), Markus B. Geuking (University of Calgary), Kathy D. McCoy (University of Calgary)
Résumé : Inosine modulates antitumor immunity Checkpoint blockade immunotherapy harnesses the immune system to kill cancer cells and has been used with great success to treat certain tumors, but not all cancer patients respond. The efficacy of checkpoint blockade immunotherapy has been shown to depend on the presence of distinct, beneficial bacteria residing in the gut of patients, but how the microbiome mediates such beneficial effects is unclear. Mager et al. found that specific bacteria produce a metabolite called inosine that enhances the effect of checkpoint blockade immunotherapy (see the Perspective by Shaikh and Sears). In mouse models, inosine, together with proinflammatory stimuli and immunotherapy, strongly enhanced the antitumor capacities of T cells in multiple tumor types, including colorectal cancer, bladder cancer, and melanoma. Science , this issue p. 1481 ; see also p. 1427