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The incorporation of the current immunotherapy, GD2-targeting monoclonal antibodies, into the standard of care has moderately improved clinical outcomes in children with high-risk neuroblastoma (HR-NB); however, overall survival remains low. More than 50% of patients with HR-NB are refractory to or eventually develop resistance to anti-GD2 treatment. HR-NBs are generally known to have a low tumor mutational burden, are immunologically cold and possess an immunosuppressive tumor microenvironment. Understanding the mechanisms of immune evasion may provide novel targets for improving the efficacy of immunotherapies for these immunologically cold HR-NBs. Here, utilizing immunocompetent mouse models of immunologically cold HR-NB, we revealed a novel function of IGF2BP1 in promoting the immune escape of neuroblastoma tumors. We demonstrate that neuroblastoma cell-specific knockdown of IGF2BP1 favorably alters the tumor microenvironment of HR-NBs, turning these "immunologically cold" tumors into an immunogenic type, thereby priming them for anti-GD2 therapy-induced immune responses. Downregulation of IGF2BP1 in NB cells decreased the number of immunosuppressive T-regulatory and dysfunctional/exhausted CD8+ T cells and promoted the accumulation of effector MHCII +  macrophages at the tumor site. Importantly, knockdown of IGF2BP1 along with anti-GD2 immunotherapy induced a synergistic immunogenic effect and achieved a potent antitumor response in an HR-NB mouse model, with increased accumulation of effector CD8+ T cells and CD86+  macrophages but decreased MDSC numbers in the tumor microenvironment. Thus, disrupting NB cancer cell IGF2BP1-mediated immunosuppression is a potential approach for improving the efficacy of anti-GD2 immunotherapy towards HR-NBs.