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However, strategies to achieve a cold\u2010to\u2010hot transition remain elusive, and suitable research models are still lacking. Here, TME profiling classifies our refractory G422\n                    <jats:sup>TN<\/jats:sup>\n                    \u2010GBM model as the TME\n                    <jats:sup>Med<\/jats:sup>\n                    (heterogeneous immune populations, \u201ccold\u201d) subtype of human GBM, which can be shifted toward the TME\n                    <jats:sup>High<\/jats:sup>\n                    (immune\u2010high, \u201chot\u201d) subtype by inhibiting TGF\u2010\u03b2 signaling. In the multi\u2010drug regimen, only \u03b1TGF\u2010\u03b2 combining temozolomide chemoradiotherapy and \u03b1PD\u20101 achieves immune\u2010cure (ICu, passing tumor rechallenge, 12.5%). ICu screening reveals a newly identified Csmd3\n                    <jats:sup>+<\/jats:sup>\n                    microglial subset with innate immune memory potential, which likely initiates durable anti\u2010GBM immune memory and closely associates with effective GBM therapy and favorable prognosis. MG\n                    <jats:sup>OE\u2022<\/jats:sup>\n                    <jats:italic>\n                      <jats:sup>Csmd3<\/jats:sup>\n                    <\/jats:italic>\n                    <jats:sup>, BV2<\/jats:sup>\n                    (\n                    <jats:italic>Csmd3<\/jats:italic>\n                    \u2010overexpressed microglial BV2) elicit robust anti\u2010GBM effects and achieve a notably 100% tumor rechallenge success in G422\n                    <jats:sup>TN<\/jats:sup>\n                    \u2010GBM mice via promoting TME\n                    <jats:sup>Med<\/jats:sup>\n                    \u2010to\u2010TME\n                    <jats:sup>High<\/jats:sup>\n                    remodeling. Taken together, our findings identify an immunologically cold TME\n                    <jats:sup>Med<\/jats:sup>\n                    GBM mouse model and provide a proof\u2010of\u2010concept for microglia\u2010based TME reprogramming and cell therapy in GBM.\n                  <\/jats:p>","DOI":"10.1002\/advs.76690","type":"journal-article","created":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T12:12:07Z","timestamp":1784549527000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Identifying a Csmd3\n                    <sup>+<\/sup>\n                    Microglial Subpopulation that Drives Cold\u2010to\u2010Hot Transition and Immune\u2010Cure in Glioblastoma"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3338-4808","authenticated-orcid":false,"given":"Hai\u2010Feng","family":"Jiang","sequence":"first","affiliation":[{"name":"Department of Pathophysiology School of Basic 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