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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE201559 | GEO | 2022/08/25

REPOSITORIES: GEO

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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.

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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]

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Histone hyperacetylation mediates enhanced IL-1β production in LPS/IFN-γ-stimulated macrophages.

Project description:Under the condition of lipopolysaccharide (LPS)/interferon (IFN)-γ activation, macrophage metabolism is converted from oxidative phosphorylation to glycolysis. In the present work, we analysed whether glycolysis could affect interleukin (IL)-1β expression through altering histone acetylation levels in mouse bone marrow-derived macrophages. Immunocytochemistry and Western blot analysis are used to characterize histone acetylation in macrophages stimulated by LPS/IFN-γ. Real-time polymerase chain reaction and enzyme-linked immunosorbent assay were used to determine IL-1β production. The metabolism of macrophages was monitored in real-time by the Seahorse test. Our results showed that glycolytic metabolism could enhance histone acetylation and promote IL-1β production in LPS/IFN-γ-activated macrophages. Moreover, increased production of IL-1β by glycolysis was mediated through enhanced H3K9 acetylation. Importantly, it was found that a high dose of histone deacetylase inhibitor could also significantly increase the expression of IL-1β in the absence of glycolytic metabolism. In conclusion, this study demonstrates that glycolytic metabolism could regulate IL-1β expression by increasing histone acetylation levels in LPS/IFN-γ-stimulated macrophages.

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IFN-gamma+ NK cells control TRAIL+ anti-inflammatory astrocytes

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

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