{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Di Luccia B"],"funding":["NCATS NIH HHS","NIDDK NIH HHS","Crohn's & Colitis Foundation","NCI NIH HHS"],"pagination":["eadi5374"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11299520"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(95)"],"pubmed_abstract":["The gut microbiota and tumor-associated macrophages (TAMs) affect tumor responses to anti-programmed cell death protein 1 (PD-1) immune checkpoint blockade. Reprogramming TAM by either blocking or deleting the macrophage receptor triggering receptor on myeloid cells 2 (TREM2) attenuates tumor growth, and lack of functional TREM2 enhances tumor elimination by anti-PD-1. Here, we found that anti-PD-1 treatment combined with TREM2 deficiency in mice induces proinflammatory programs in intestinal macrophages and a concomitant expansion of <i>Ruminococcus gnavus</i> in the gut microbiota. Gavage of wild-type mice with <i>R. gnavus</i> enhanced anti-PD-1-mediated tumor elimination, recapitulating the effect occurring in the absence of TREM2. A proinflammatory intestinal environment coincided wit"],"journal":["Science immunology"],"pubmed_title":["TREM2 deficiency reprograms intestinal macrophages and microbiota to enhance anti-PD-1 tumor immunotherapy."],"pmcid":["PMC11299520"],"funding_grant_id":["P30 CA091842","R01 CA262684","R00 DK118110","UL1 TR002345","R01 DK119147","938100","P30 DK056341"],"pubmed_authors":["Chang HW","Trsan T","Onufer EJ","Molgora M","Colonna M","Czepielewski RS","da Silva CS","Di Luccia B","Helmink BA","Gilfillan S","Gordon JI","Fachi JL","Hou J","Jaeger N","Cella M","Khantakova D","Bando JK","Bhattarai B","Schreiber RD","Rodrigues PF"],"additional_accession":[]},"is_claimable":false,"name":"TREM2 deficiency reprograms intestinal macrophages and microbiota to enhance anti-PD-1 tumor immunotherapy.","description":"The gut microbiota and tumor-associated macrophages (TAMs) affect tumor responses to anti-programmed cell death protein 1 (PD-1) immune checkpoint blockade. Reprogramming TAM by either blocking or deleting the macrophage receptor triggering receptor on myeloid cells 2 (TREM2) attenuates tumor growth, and lack of functional TREM2 enhances tumor elimination by anti-PD-1. Here, we found that anti-PD-1 treatment combined with TREM2 deficiency in mice induces proinflammatory programs in intestinal macrophages and a concomitant expansion of <i>Ruminococcus gnavus</i> in the gut microbiota. Gavage of wild-type mice with <i>R. gnavus</i> enhanced anti-PD-1-mediated tumor elimination, recapitulating the effect occurring in the absence of TREM2. A proinflammatory intestinal environment coincided wit","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-01T07:17:30.591Z","creation":"2025-04-06T22:44:24.443Z"},"accession":"S-EPMC11299520","cross_references":{"pubmed":["38758808"],"doi":["10.1126/sciimmunol.adi5374"]}}