dc.contributor.author | Pires-Afonso, Yolanda | |
dc.contributor.author | Muller, Arnaud | |
dc.contributor.author | Grzyb, Kamil | |
dc.contributor.author | Oudin, Anaïs | |
dc.contributor.author | Yabo, Yahaya A. | |
dc.contributor.author | Sousa, Carole | |
dc.contributor.author | Scafidi, Andrea | |
dc.contributor.author | Poli, Aurélie | |
dc.contributor.author | Cosma, Antonio | |
dc.contributor.author | Halder, Rashi | |
dc.contributor.author | Coowar, Djalil | |
dc.contributor.author | Golebiewska, Anna | |
dc.contributor.author | Skupin, Alexander | |
dc.contributor.author | Niclou, Simone Pierrette | |
dc.contributor.author | Michelucci, Alessandro | |
dc.date.accessioned | 2023-03-15T12:46:34Z | |
dc.date.available | 2023-03-15T12:46:34Z | |
dc.date.created | 2022-10-24T19:54:52Z | |
dc.date.issued | 2022 | |
dc.identifier.issn | 1574-7891 | |
dc.identifier.uri | https://hdl.handle.net/11250/3058430 | |
dc.description.abstract | In glioblastoma (GBM), tumour-associated microglia/macrophages (TAMs) represent the major cell type of the stromal compartment and contribute to tumour immune escape mechanisms. Thus, targeting TAMs is emerging as a promising strategy for immunotherapy. However, TAM heterogeneity and metabolic adaptation along GBM progression represent critical features for the design of effective TAM-targeted therapies. Here, we comprehensively study the cellular and molecular changes of TAMs in the GL261 GBM mouse model, combining single-cell RNA-sequencing with flow cytometry and immunohistological analyses along GBM progression and in the absence of Acod1 (also known as Irg1), a key gene involved in the metabolic reprogramming of macrophages towards an anti-inflammatory phenotype. Similarly to patients, we identify distinct TAM profiles, mainly based on their ontogeny, that reiterate the idea that microglia- and macrophage-like cells show key transcriptional differences and dynamically adapt along GBM stages. Notably, we uncover decreased antigen-presenting cell features and immune reactivity in TAMs along tumour progression that are instead enhanced in Acod1-deficient mice. Overall, our results provide insight into TAM heterogeneity and highlight a novel role for Acod1 in TAM adaptation during GBM progression. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Wiley | en_US |
dc.rights | Navngivelse 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/deed.no | * |
dc.title | Elucidating tumour-associated microglia/macrophage diversity along glioblastoma progression and under ACOD1 deficiency | en_US |
dc.type | Journal article | en_US |
dc.type | Peer reviewed | en_US |
dc.description.version | publishedVersion | en_US |
dc.rights.holder | Copyright 2022 The Author(s) | en_US |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |
dc.identifier.doi | 10.1002/1878-0261.13287 | |
dc.identifier.cristin | 2064630 | |
dc.source.journal | Molecular Oncology | en_US |
dc.source.pagenumber | 3167-3191 | en_US |
dc.identifier.citation | Molecular Oncology. 2022, 16 (17), 3167-3191. | en_US |
dc.source.volume | 16 | en_US |
dc.source.issue | 17 | en_US |