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Oncolytic Zika virus (ZIKV) has emerged as a promising therapy, targeting treatment-resistant glioma stem cells, stimulating CD8+ T-cell-mediated immunity and extends survival in preclinical models but myeloid cell-driven immunosuppression persists. An antagonist of Siglec-15, a myeloid immune checkpoint molecule, is in a phase II trial for non-small cell lung cancer, but its role in CNS malignancies remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We evaluated Siglec-15 expression in human GBM samples using flow cytometry, mass cytometry, and immunofluorescence, as well as a public database. Using syngeneic glioma models, we tested a blocking antibody against Siglec-15, and Siglec-15 knockout mice, alongside ZIKV and anti-PD-1 therapies. We performed survival studies and analyzed immune responses, T-cell proliferation and phagocytosis, and tumor rechallenge.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Siglec-15 was expressed by human GBM myeloid (16%-22%) and tumor (18%-19%) cells, and higher expression was associated with shorter survival. In CT2A-bearing mice, ZIKV\u2009+\u2009anti-Siglec-15 increased long-term survival to 60% (vs 40% with ZIKV alone), rising to 83% with anti-PD-1 treatment. Triple therapy in SB28 bearing mice yielded 76% long-term survivor rate with 1.7-fold higher CD8+ T-cell activation. Rechallenged mice showed 11-fold expansion of brain resident\/effector memory CD8+ T cells and 80% survival. Siglec-15 loss on myeloid cells enhanced phagocytosis (CT2A: 25%; SB28: 7%) and T-cell responses (activation: 81%; proliferation: 86.8%).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Targeting Siglec-15, combined with PD-1 blockade and ZIKV overcomes myeloid immunosuppression and enhances T-cell activation in GBM, promoting durable antitumor immunity. These findings support further investigation of this combination therapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/neuonc\/noag186","type":"journal-article","created":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T11:13:31Z","timestamp":1786101211000},"source":"Crossref","is-referenced-by-count":0,"title":["Siglec-15 and PD-1 checkpoint blockade in combination with oncolytic Zika virus infection confers protection against immune-resistant gliomas"],"prefix":"10.1093","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4008-6289","authenticated-orcid":false,"given":"Ashwani","family":"Kesarwani","sequence":"first","affiliation":[{"name":"Department of Medicine, Washington University School of Medicine , St. Louis, Missouri,","place":["USA"]},{"name":"The Brain Tumor Center, Alvin J. 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