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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [CT2A]

ABSTRACT: CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [CT2A]

PROVIDER: PRJNA832218 | ENA |

REPOSITORIES: ENA

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	SRR18923396.fastq.gz	Fastqsanger.gz

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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [CT2A]

Project description:Therapies against glioblastoma multiforme (GBM) have been largely ineffective due to the infiltration of immunosuppressive tumor-associated macrophages (TAMs). Recent studies demonstrated that TAMs can also be immune-activating. However, markers differentiating these heterogeneous macrophage populations have not been established. In this study, we identified a subset of macrophages expressing CD169 that promote an anti-tumoral microenvironment in GBM. Using single-cell transcriptome analysis, we found that CD169+ macrophages in human and mouse gliomas produced proinflammatory chemokines, leading to the accumulation of T cells and NK cells. Depletion of CD169+ macrophages shortened the survival of mice with gliomas and reduced the function of antitumor lymphocytes. We show that IFN-γ produced by NK cells was critical for the accumulation of CD169+ macrophages into gliomas. Additionally, CD169 expression on macrophages increased the phagocytosis of apoptotic glioma cells. Our finding suggests that the CD169+ subset of TAMs promotes antitumor immune responses against GBM.

2022-09-11 | GSE201553 | GEO

CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [EGFRviii]

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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [WG vs TG]

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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor

Project description:CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor

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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [EGFRviii]

Project description:CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [EGFRviii]

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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [WG vs TG]

Project description:CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [WG vs TG]

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CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-25 | GSE201559 | GEO

Effects of the treatment with IFNβ and GM-CSF-secreting CT2A cells to wildtype CT2A tumor microenvironment post resection

Project description:To elucidate the underlying immune responses elicited by IFNβ and GM-CSF-secreting CT2A cells to brain tumor microenvironment post resection compared to placebo group and non-IFNβ and GM-CSF-secreting CT2A cell group

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Transcriptional profiling of Cd169-lineage lymph node macrophages

Project description:Tingible body macrophages (TBMs) exist in lymph node B cell follicles and are responsible for clearing apoptotic B cells. Our data suggests that TBMs are of Cd169-lineage. We isolated cells from Cd169Cre/+.Tdtomatofl/fl reporter mice and transcriptionally profiled them to identify putative TBMs and chacterise their development and function relative to other LN cells of the Cd169 lineage.

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Antigen presentation deficiency, mesenchymal differentiation, and resistance to immunotherapy in the murine syngeneic CT2A tumor model

Project description:A common cornerstone of preclinical cancer research is the use of syngeneic orthotopic murine tumors as immunocompetent models of human cancers. For glioblastoma research efforts, the GL261 and CT2A lines are frequently used. We systematically characterized these two lines to decipher the cell-intrinsic mechanisms that drive immuno-resistance in CT2A and to define the aspects of human cancer biology that the lines best model. We show that, despite sharing a few canonical genetic or histologic features of human glioblastoma, the transcriptional profiles of GL261 and CT2A tumours most closely resembled those of glioblastomas. CT2A additionally resembled other cancer types transcriptionally, including melanoma. CT2A displayed mesenchymal differentiation, upregulated angiogenesis, and multiple defects in antigen presentation machinery and interferon response pathways. Loss of MHC class I expression was restored in CT2A by interferon-γ treatment, explaining in part the modest efficacy of some immunotherapy combinations for CT2A. Our findings indicate that CT2A may serve as a robust preclinical solid tumor model of adaptive immune resistance.

2023-12-19 | PXD036720 | Pride

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