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Immunotherapy efficacy in colorectal cancer is dependent on activation of a microbial-metabolite-immune circuit

Mager, L.; Burkhard, R.; Cooke, N.; Brown, K.; Ramay, H.; Paik, S.; Stagg, J.; Grooves, R.; Gallo, M.; Lewis, I.; Geuking, M.; McCoy, K.

2020-02-27 cancer biology
10.1101/2020.02.26.965533 bioRxiv
Show abstract

Cancer is a leading cause of death globally. Checkpoint blockade therapies offer a promising treatment for many cancers, but have been ineffective for colorectal cancers. Previous studies have shown a dependency of immunotherapies on the microbiota. Consequently, we hypothesized that specific gut bacteria promote immunotherapy for colorectal cancer. We identify three commensal bacteria and a microbial metabolite, inosine, that enhance the efficacy of immune checkpoint blockade therapy in colorectal cancer. We show that inosine interacts with the adenosine A2A receptor on T cells resulting in intestinal Th1 cell differentiation. Decreased gut barrier function induced by immunotherapy increased the translocation of bacterial metabolites and promoted cancer protective Th1 cell activation. This microbial-metabolite-immune circuit provides a mechanism for a new class of bacteria-enhanced checkpoint blockade therapies. The efficacy of this mechanism differs among colorectal cancer subtypes and highlights the strengths as well as potential limitations of this novel bacterial co-therapy for cancer.

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