{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nejo T"],"funding":["NCI NIH HHS","NINDS NIH HHS","NIH HHS"],"pagination":["4770"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12098748"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Neuronal activity-driven mechanisms influence glioblastoma cell proliferation and invasion, while glioblastoma remodels neuronal circuits. Although a subpopulation of malignant cells enhances neuronal connectivity, their impact on the immune system remains unclear. Here, we show that glioblastoma regions with enhanced neuronal connectivity exhibit regional immunosuppression, characterized by distinct immune cell compositions and the enrichment of anti-inflammatory tumor-associated macrophages (TAMs). In preclinical models, knockout of Thrombospondin-1 (TSP1/Thbs1) in glioblastoma cells suppresses synaptogenesis and glutamatergic neuronal hyperexcitability. Furthermore, TSP1 knockout restores antigen presentation-related genes, promotes the infiltration of pro-inflammatory TAMs and CD8 + T-"],"journal":["Nature communications"],"pubmed_title":["Glioma-neuronal circuit remodeling induces regional immunosuppression."],"pmcid":["PMC12098748"],"funding_grant_id":["P50 CA097257","K08 NS110919","P30 CA082103","R35 NS105068","R01 NS137950","S10 OD028511","T32 CA151022","K08 NS126573"],"pubmed_authors":["Gallus M","Okada H","Lakshmanachetty S","Okada K","Cadwell CR","Phyu SSS","Nejo T","Baker DL","Lee KY","Phung L","Maldonado GC","Jimenez C","Yamamichi A","Diebold D","Ogino H","Young JS","Hervey-Jumper SL","Krishna S","Daniel AGS","Raleigh DR","Choudhury A","Chen T","Watchmaker PB"],"additional_accession":[]},"is_claimable":false,"name":"Glioma-neuronal circuit remodeling induces regional immunosuppression.","description":"Neuronal activity-driven mechanisms influence glioblastoma cell proliferation and invasion, while glioblastoma remodels neuronal circuits. Although a subpopulation of malignant cells enhances neuronal connectivity, their impact on the immune system remains unclear. Here, we show that glioblastoma regions with enhanced neuronal connectivity exhibit regional immunosuppression, characterized by distinct immune cell compositions and the enrichment of anti-inflammatory tumor-associated macrophages (TAMs). In preclinical models, knockout of Thrombospondin-1 (TSP1/Thbs1) in glioblastoma cells suppresses synaptogenesis and glutamatergic neuronal hyperexcitability. Furthermore, TSP1 knockout restores antigen presentation-related genes, promotes the infiltration of pro-inflammatory TAMs and CD8 + T-","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-02T20:46:39.22Z","creation":"2026-04-20T03:14:20.341Z"},"accession":"S-EPMC12098748","cross_references":{"pubmed":["40404658"],"doi":["10.1038/s41467-025-60074-z"]}}