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Immune checkpoint blockade induces gut microbiota translocation that augments extraintestinal antitumor immunity
Yongbin Choi (The University of Texas Southwestern Medical Center), Jake N. Lichterman (The University of Texas Southwestern Medical Center), Laura A. Coughlin (The University of Texas Southwestern Medical Center), Nicole A. Poulides (The University of Texas Southwestern Medical Center), Wenling Li (The University of Texas Southwestern Medical Center), Priscilla Del Valle (The University of Texas Southwestern Medical Center), Suzette N. Palmer (The University of Texas Southwestern Medical Center), Shuheng Gan (The University of Texas Southwestern Medical Center), Jiwoong Kim (The University of Texas Southwestern Medical Center), Xiaowei Zhan (The University of Texas Southwestern Medical Center), Yajing Gao (The University of Texas Southwestern Medical Center), Bret M. Evers (The University of Texas Southwestern Medical Center), Lora V. Hooper (Howard Hughes Medical Institute, The University of Texas Southwestern Medical Center), Chandrashekhar Pasare (Cincinnati Children's Hospital Medical Center, University of Cincinnati), Andrew Young Koh (Harold C. Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center)
Résumé : Gut microbiota, specifically gut bacteria, are critical for effective immune checkpoint blockade therapy (ICT) for cancer. The mechanisms by which gut microbiota augment extraintestinal anticancer immune responses, however, are largely unknown. Here, we find that ICT induces the translocation of specific endogenous gut bacteria into secondary lymphoid organs and subcutaneous melanoma tumors. Mechanistically, ICT induces lymph node remodeling and dendritic cell (DC) activation, which facilitates the translocation of a selective subset of gut bacteria to extraintestinal tissues to promote optimal antitumor T cell responses in both the tumor-draining lymph nodes (TDLNs) and the primary tumor. Antibiotic treatment results in decreased gut microbiota translocation into mesenteric lymph nodes (MLNs) and TDLNs, diminished DC and effector CD8 + T cell responses, and attenuated responses to ICT. Our findings illuminate a key mechanism by which gut microbiota promote extraintestinal anticancer immunity.