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Enterococcus peptidoglycan remodeling promotes checkpoint inhibitor cancer immunotherapy
Matthew E. Griffin (Scripps Research Institute, Rockefeller University), Juliel Espinosa (Rockefeller University), Jessica L. Becker (Rockefeller University), Ji‐Dung Luo (Rockefeller University), Thomas S. Carroll (Rockefeller University), Jyoti K. Jha, Gary R. Fanger, Howard C. Hang (Scripps Research Institute, Rockefeller University)
Résumé : SagA promotes immunotherapy response The gut microbiome can influence the treatment outcome for cancer patients receiving PD-L1 immunotherapy, but the mechanisms underlying favorable responses are unclear. Griffin et al . found that a particular type of bacteria called enterococci enhance anti–PD-L1 immunotherapy in mice (see the Perspective by Ansaldo and Belkaid). The researchers show that enterococci secrete an enzyme called SagA that breaks down components of the bacterial cell wall. This process results in the release of muramyl peptide fragments, which in turn act as stimulatory molecules to promote signaling of the innate immune sensor protein NOD2 and improved immunotherapy responses. —PNK