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The mechanisms constraining this systemic immune response remain poorly understood. This study investigates galectin-9 (Gal-9), a ligand for the TIM-3 (T-cell immunoglobulin and mucin-domain containing-3) immune checkpoint, as a mediator of immune escape that limits RT systemic efficacy and evaluates combinatorial RT\/Gal-9 blockade in preclinical models.<\/jats:p>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Multiplatform analysis (RNA sequencing, immunoblot, flow cytometry, ELISA, immunohistochemistry) characterized RT-induced Gal-9 regulation in human lung\/colorectal cancer cell lines, murine tumors\/serums, and paired patient tumors. Local and abscopal therapeutic efficacy was evaluated in homologous (CT26\/CT26, LLC\/LLC) and heterologous (CT26\/4T1) two-tumor mouse models. Immune profiling of tumor microenvironment, tumor-draining lymph nodes (tdLNs), and splenic compartments was comprehensively assessed by flow cytometry. Mechanistic studies employed STING (Stimulator of Interferon Genes) inhibition (H151), CD8\n                      <jats:sup>+<\/jats:sup>\n                      T-cell depletion (anti-CD8\u03b1), macrophage\/monocyte depletion (PLX-3397), interferon-I (IFN-I) blockade (anti-IFNAR1), and lymphocyte egress inhibition (FTY720).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      RT upregulated Gal-9 predominantly within host myeloid compartments (dendritic cells, macrophages, monocytes, neutrophils) versus tumor cells, in both irradiated tumors and abscopal tumors. Mechanistically, RT-activated STING-IFN-I axis locally induced Gal-9\n                      <jats:sup>+<\/jats:sup>\n                      myeloid cells that subsequently disseminated systemically. Clinically, elevated post-RT Gal-9 in patient biopsies correlated with poor therapeutic outcomes. Notably, combining Gal-9 blockade with RT elicited potent abscopal responses in homologous two-tumor mouse models. Furthermore, anti-Gal-9 markedly enhanced radio-immunotherapy efficacy in the poorly immunogenic Lewis lung carcinoma. Immunologically, Gal-9 blockade synergized with RT to activate the myeloid and T cell compartments, enhancing dendritic cell accumulation in tdLNs and boosting CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cell infiltration in abscopal tumors. Depletion of CD8\n                      <jats:sup>+<\/jats:sup>\n                      T cells\/monocytes or blocking lymphocyte egress from lymph nodes abrogated the abscopal efficacy, underscoring their essential roles.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings establish RT-induced Gal-9 as a novel dual myeloid\/T-cell immune checkpoint restricting abscopal responses. Gal-9 blockade represents a promising strategy to potentiate radiotherapy against metastatic disease, defining a therapeutic paradigm distinct from conventional checkpoint inhibitors.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2025-013675","type":"journal-article","created":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T13:30:22Z","timestamp":1783085422000},"page":"e013675","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Galectin-9-driven immune evasion constrains radiotherapy-induced systemic antitumor immunity"],"prefix":"10.1136","volume":"14","clinical-trial-number":[{"clinical-trial-number":"nct04666688","registry":"10.18810\/clinical-trials-gov"}],"author":[{"given":"Jiaming","family":"Song","sequence":"first","affiliation":[{"name":"Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, 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