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Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [RNA-seq.Mouse]

ABSTRACT: We investigated the mechanism of suppression of Notch during efferocytosis. Genetically activation of Notch or ablation of Rubicon in marophages induced pro-inflammatory polarization and enhance anti-tumor effect.

ORGANISM(S): Mus musculus

PROVIDER: GSE283548 | GEO | 2026/01/08

REPOSITORIES: GEO

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Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [RNA-seq.HumanMouse]

Project description:We investigated the mechanism of suppression of Notch during efferocytosis. Genetically activation of Notch or ablation of Rubicon in marophages induced pro-inflammatory polarization and enhance anti-tumor effect.

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Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [SLAM-seq]

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Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization

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Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [SLAM-seq]

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Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [RNA-seq.Mouse]

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Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization [RNA-seq.HumanMouse]

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Suppression of Notch during efferocytosis prevents macrophages inflammatory polarization

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

2026-01-08 | GSE283550 | GEO

The Second Generation of CAR-iMACs with Enhanced Polarization, CAR-mediated Efferocytosis and Superior Potency against Solid Tumors

Project description:Chimeric antigen receptor (CAR)-T cell therapies have shown great success in treating hematologic malignancies. Nonetheless, their therapeutic effect on solid tumors remains to be improved. Recently, macrophages have attracted great attention, given their ability to infiltrate solid tumors, phagocytize tumor cells as well as their immunomodulatory capacities. The first generation of CD3ζ-based CAR-macrophages demonstrated that the CAR could stimulate macrophage phagocytosis in a tumor antigen-dependent way. Here, we genetically engineered induced pluripotent stem cell (iPSC)-derived macrophages (iMACs) with TLR4 intracellular TIR domain-containing CARs against EGFRvIII and GPC3, which yielded markedly enhanced antitumor effect in two different solid tumor models including glioblastoma, and hepatocellular carcinoma in which complete remission was achieved with CAR-iMACs alone or in combination with CD47 antibody. Moreover, the tandem CD3ζ-TIR-CAR, or the “second-generation” design of TIR-based dual signaling CAR, endowed iMACs with both target engulfment/efferocytosis capacity against antigen-expressing solid tumor cells, and potency of antigen-dependent M1 state polarization and M2 state resistance in an NF-κB dependent manner. We also illustrated a surprising mechanism of tumor cell elimination by CAR-induced efferocytosis against tumor cell apoptotic bodies. Taken together, we established the next generation CAR-iMACs equipped with orthogonal phagocytosis and polarization capacity for better antitumor functions in treating solid tumors.

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miRNA regulated by Notch signaling in macrophage

Project description:This two-color miRNA chip was perfored to identify the downstream miRNAs regulated by Notch signaling in macrophage polarization. To identify the downstream miRNAs mediated by Notch signaling during macrophage polarization regulating, RNA was isolated from bone marrow drived macrophages (BMDMs) of Notch signaling deletion and wild type mice as experiment samples. Three control (+/-) and three experiment (-/-) samples were detected.

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Study of human macrophage reprogramming toward a pro-resolving profile by efferocytosis

Project description:Inﬂammation is a physiopathological process triggered by infection or tissue damage. Immune system initiates coordinated sequential steps in response to these danger signals. Once the threat has been contained inflammation has to be subsequently shut down. Inflammation resolution is initiated by the reprogramming of pro-inflammatory macrophages toward a pro-resolving profile. This reprogramming is induced in particular by the non-phlogistic engulfment of apoptotic cells, mostly apoptotic neutrophils, a process called efferocytosis. As a matter of fact, macrophages are an essential linchpin regulating both inflammation triggering and sustaining and inflammation resolution. This duality can be achieved through the tremendous plasticity of these innate immune cells. Indeed, depending on microenvironmental signals (cytokines, efferocytosis, growth factors…) macrophages can adopt numerous diverse and sometimes antagonistic phenotypes. The mechanisms governing these transitions remain relatively scattered especially in human. With this project we propose to explore the mechanisms involved in human macrophage reprogramming toward a pro-resolving profile after efferocytosis. The stakes are high due to the estimated prevalence of chronic inflammatory diseases in Western society is 5 to 7%. Chronic inflammation is a burden to patient due to life-long debilitating illness and increased mortality and is also a burden to society due to high costs for therapy and care. Finding new therapies to limit chronic inflammation establishment and persistence is thus a highly valuable goal.

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