{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:28:22Z","timestamp":1792787302494,"version":"4.5.0"},"reference-count":69,"publisher":"BMJ","issue":"9","license":[{"start":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T00:00:00Z","timestamp":1788307200000},"content-version":"unspecified","delay-in-days":1,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"National Science Foundation of China","award":["82170173"],"award-info":[{"award-number":["82170173"]}]},{"name":"National Science Foundation of China","award":["82371789"],"award-info":[{"award-number":["82371789"]}]},{"name":"Tianjin Medical University Talent Program","award":["U25A2050"],"award-info":[{"award-number":["U25A2050"]}],"id":[{"id":"https:\/\/ror.org\/02mh8wx89","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["J Immunother Cancer"],"accepted":{"date-parts":[[2026,8,19]]},"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Tumor-associated macrophages (TAMs) play pivotal roles in shaping the tumor-microenvironment (TME) through functional plasticity, which is regulated by extrinsic and intrinsic signals. However, the role of vesicular trafficking in TAMs remains poorly understood. RAB31, a small GTPase enriched in myeloid cells, was proposed as a potential regulator of TAM polarization through clathrin-mediated endocytosis (CME). We hypothesized that RAB31 modulates TAM education by tumor-derived signals and thereby shapes antitumor immunity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We profiled RAB31 expression in human cancers using public single-cell RNA sequencing (scRNA-seq) datasets and clinical sample immunofluorescence staining. Rab31 knockout mice were employed in subcutaneous tumor models. The TME was profiled by scRNA-seq, bulk RNA-seq, and flow cytometry. Bone marrow transplantation, adoptive cell transfer, and antibody-mediated depletion were performed to identify the effector cell populations. Co-immunoprecipitation coupled with mass spectrometry, receptor half-life assays, inhibitor intervention and lysosomal colocalization experiments dissected the molecular mechanism. Functional T-cell chemotaxis, activation, and anti-programmed death-ligand 1 (PD-L1) response assays were performed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      RAB31 was highly expressed in TAMs across multiple cancers and correlated with poor prognosis and immunosuppressive TME. Rab31 deficiency reprogrammed TAMs to M1-like phenotype, enhanced CD8\n                      <jats:sup>+<\/jats:sup>\n                      T-cell infiltration and activation, and suppressed tumor growth. Mechanistically, Rab31 preserves FPR2 cell surface stability through a CME-dependent mechanism; its loss redirected FPR2 to lysosomal degradation, disrupted tumor-derived ANXA1 signaling, and unleashed NF-\u03baB activity. Rab31 deficiency synergized with anti-PD-L1 therapy in a CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cell-dependent manner.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings establish the CME\/RAB31 pathway as an indispensable regulator of TAM polarization, underscoring the pivotal role of vesicular trafficking in the TME.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2026-015703","type":"journal-article","created":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T15:05:13Z","timestamp":1788361513000},"page":"e015703","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["GTPase RAB31 supports ANXA1-driven macrophage education through clathrin-mediated endocytosis to suppress antitumor 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