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TREM1 deficiency alters the tumor myeloid landscape

ABSTRACT: TREM1 deficiency alters the tumor myeloid landscape

PROVIDER: PRJEB65047 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR11829083_1.fastq.gz	Fastqsanger.gz
	ERR11829083_2.fastq.gz	Fastqsanger.gz
	ERR11829085_1.fastq.gz	Fastqsanger.gz
	ERR11829085_2.fastq.gz	Fastqsanger.gz

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TREM1 deficiency alters the tumor myeloid landscape

Project description:To comprehensively characterize the impact of TREM1 deficiency specifically within the tumor myeloid populations, we selectively enriched the CD45+CD11b+ tumor-infiltrating myeloid cells from tumor-bearing Trem1+/+ and Trem1-/- mice for scRNA-seq analysis.

2023-09-27 | E-MTAB-13246 | biostudies-arrayexpress

Myeloid BAF60a Deficiency Alters Metabolic Homeostasis and Exacerbates Atherosclerosis

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Differential gene expression in TREM1 -/- vs +/+ myeloid cells 48h after MCAo-RP

Project description:Stroke is a multiphasic progress characterized by neuron damage due to hypoxia followed by secondary damage from the subsequent inflammatory immune response. Infiltrating myeloid cells induce cerebral damage through pro-inflammatory cytokines, chemokines, proteases and generation of reactive oxygen species (ROS). Triggering receptor expressed on myeloid cells 1 (TREM1) is exclusively expressed on myeloid cells and acts as an amplifier of pro-inflammatory innate immune responses. Using microarray analysis, we aim to identify the expression differences and functional change of these myeloid cells after TREM1 knockout in mice post stroke.

2019-07-02 | GSE105132 | GEO

Identification of TREM1+CD163+ myeloid cells as a deleterious immune subset in HCC [Spatial Transcriptomics]

Project description:Hepatocellular carcinoma (HCC) is an inflammation-associated cancer arising from viral and non-viral etiologies. Expansion of suppressive myeloid cells is a hallmark of chronic inflammation and cancer, but their heterogeneity in HCC is not fully resolved and might underlie immunotherapy resistance in the steatohepatitis setting. Here, we present a high resolution atlas of hepatic innate immune cells from patients with HCC that unravels a steatohepatitis contexture characterized by influx of inflammatory and immunosuppressive myeloid cells. A discrete myeloid cell population identified by selective expression of TREM1 and CD163 expands in steatohepatitis-HCC. We refer to this population as TREM1+ regulatory myeloid cells (Mreg), as it potently suppresses T cell effector functions, highly expresses TGFB1 and IL13RA1 and localizes to HCC fibrotic lesions.

2024-02-04 | GSE245908 | GEO

Identification of TREM1+CD163+ myeloid cells as a deleterious immune subset in HCC [scRNA-seq]

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Identification of TREM1+CD163+ myeloid cells as a deleterious immune subset in HCC [bulk_RNA-seq]

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scRNA seq analysis of CD45+ tumor infiltrating cells (TICs) of B16F10 tumor-bearing Trem1+/+ and Trem1-/- mice.

Project description:To gain a global understanding of the impact of TREM1 silencing, we analyzed the CD45+ tumor infiltrating cells (TICs) of B16F10 tumor-bearing Trem1+/+ and Trem1-/- mice. Utilizing the 10x Genomics Chromium Platform, we analyzed approximately 5390 cells per sample with a coverage rate of 15493 genes per cell.

2023-09-27 | E-MTAB-13237 | biostudies-arrayexpress

Differential gene expression in TREM1 -/- vs +/+ myeloid cells 48h after MCAo-RP

Project description:Differential gene expression in TREM1 -/- vs +/+ myeloid cells 48h after MCAo-RP

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Identification of TREM1+CD163+ myeloid cells as a deleterious immune subset in HCC

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Vitamin D deficiency during development permanently alters liver cell composition and function.

Project description:Vitamin D, a fat-soluble vitamin, plays a critical role in calcium homeostasis, the immune system, and normal development. Many epidemiological cohort studies globally have found high prevalence rates of vitamin D deficiency and insufficiency, recognized as an important health issue that needs to be solved. In particular, reproductive age and pregnant women low in vitamin D status may confer risks of diseases like obesity on their offspring. While observational studies have suggested associations between prenatal vitamin D deficiency and metabolic phenotypes in offspring, not yet determined is whether prenatal vitamin D deficiency permanently alters the development of the liver, a major metabolic organ. We tested the histopathology and the transcriptomic profiles of livers from male C57BL/6J mice exposed to prenatal vitamin D deficiency through a maternal dietary intervention model. We found that prenatal vitamin D deficiency increases the prevalence of histopathological changes in the liver, and alters its gene expression profile. Cell subtype proportion analysis showed that the liver of prenatal vitamin D deficiency alters non-parenchymal cells of the liver, specifically macrophages, a subset of endothelial cells, and dendritic cells. Our results indicate the long-term memory of prenatal vitamin D deficiency exposure in the adult liver, a potential contributor to offspring health risks.

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