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However, the specific microbial determinants, underlying mechanisms, and potential clinical applications remain incompletely elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Building on the observed association between gut microbiota and anti-programmed cell death protein-1 (PD-1) immunotherapeutic efficacy in patients with hepatocellular carcinoma (HCC), we leveraged a suite of clinically relevant murine HCC models to comprehensively characterize tumor-associated microbial signatures using 16S ribosomal RNA gene sequencing. By precisely manipulating microbial composition through a non-hepatotoxic antibiotic cocktail 3 (ABX-3), targeted microbial supplementation, human fecal microbiota transplant (FMT), and controlled\n                      <jats:italic>Bacteroides thetaiotaomicron (B.th<\/jats:italic>\n                      ) repopulation following gut sterilization with ABX-5, we demonstrated a direct causal relationship between microbiota modulation and intrahepatic immune activation. Single-cell RNA sequencing of hepatic non-parenchymal cells, together with functional validation experiments, was performed to elucidate the underlying immune mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Bacteroides<\/jats:italic>\n                      -enriched gut microbiota derived from anti-PD-1-responsive patients with HCC significantly suppressed tumor growth in murine HCC models. In parallel, within our murine HCC system, ABX-3 administration, implemented as both a preventive and therapeutic intervention, attenuated tumor initiation and progression by selectively enriching\n                      <jats:italic>Bacteroides<\/jats:italic>\n                      within the gut microbial community. Functionally, ABX-3 enhanced the capacity of tumor antigen-specific T-cell receptor-I T cells to mount robust immune responses, culminating in targeted tumor regression following antigen-specific immunization. Among the\n                      <jats:italic>Bacteroides<\/jats:italic>\n                      species,\n                      <jats:italic>B.th<\/jats:italic>\n                      emerged as a critical mediator that potentiated \u03b1PD-1 immunotherapy in HCC by relieving Kr\u00fcppel-like factor 2 (KLF2)-dependent suppression in dendritic cells (DCs). Mechanistically, the KLF2\u2013toll-like receptor 9 (TLR9) signaling axis in DCs governed the activation of antigen-specific CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells, thereby amplifying antitumor immunity within the HCC microenvironment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:italic>B.th<\/jats:italic>\n                      is identified as a key immunomodulatory species that enhances anti-PD-1 efficacy by reprogramming DCs through the KLF2\/TLR9 signaling pathway. These findings reveal a novel microbiota-informed strategy to improve immunotherapeutic outcomes in HCC.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2025-013755","type":"journal-article","created":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T13:45:27Z","timestamp":1771335927000},"page":"e013755","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":5,"title":["Modulating\n                    <i>Bacteroides<\/i>\n                    to boost anti-PD-1 immunotherapy in HCC"],"prefix":"10.1136","volume":"14","author":[{"given":"Xiaoqiang","family":"Qi","sequence":"first","affiliation":[{"name":"Department of Surgery, University of Missouri, Columbia, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4895-5864","authenticated-orcid":false,"given":"Ming","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Missouri, Columbia, Missouri, USA"},{"name":"Department of Surgery, UConn Health Center, Farmington, Connecticut, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1109-1740","authenticated-orcid":false,"given":"Xinjian","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Missouri, Columbia, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2171-1226","authenticated-orcid":false,"given":"Lixin","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Radiology, University of Missouri, Columbia, Missouri, USA"},{"name":"Harry S. 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