Journal
SCIENCE
Volume 342, Issue 6161, Pages 971-976Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1240537
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Funding
- Institut National du Cancer (INCa)
- la Ligue contre le cancer (LIGUE labelisee)
- SIRIC Socrates
- LABEX
- PACRI Onco-Immunology
- European Research Council [202283]
- NIH [P01DK071176]
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Cyclophosphamide is one of several clinically important cancer drugs whose therapeutic efficacy is due in part to their ability to stimulate antitumor immune responses. Studying mouse models, we demonstrate that cyclophosphamide alters the composition of microbiota in the small intestine and induces the translocation of selected species of Gram-positive bacteria into secondary lymphoid organs. There, these bacteria stimulate the generation of a specific subset of pathogenic T helper 17 (pT(H)17) cells and memory T(H)1 immune responses. Tumor-bearing mice that were germ-free or that had been treated with antibiotics to kill Gram-positive bacteria showed a reduction in pT(H)17 responses, and their tumors were resistant to cyclophosphamide. Adoptive transfer of pT(H)17 cells partially restored the antitumor efficacy of cyclophosphamide. These results suggest that the gut microbiota help shape the anticancer immune response.
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