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EGR2 is required for the acquisition of hLAM phenotype by monocyte-derived macrophages in MASH.

ABSTRACT: EGR2 is required for the acquisition of hLAM phenotype by monocyte-derived macrophages in MASH.

PROVIDER: PRJNA1100494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28699866_1.fastq.gz	Fastqsanger.gz
	SRR28699866_2.fastq.gz	Fastqsanger.gz
	SRR28699867_1.fastq.gz	Fastqsanger.gz
	SRR28699867_2.fastq.gz	Fastqsanger.gz
	SRR28699868_1.fastq.gz	Fastqsanger.gz

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EGR2 is required for the acquisition of hLAM phenotype by monocyte-derived macrophages in MASH.

Project description:This analysis was performed to understand the difference between WT and EGR2 KO macrophages in MASH liver.

2024-05-02 | GSE263974 | GEO

EGR2 is upregulated in monocyte-derived macrophages in MASH liver

Project description:EGR2 is upregulated in monocyte-derived macrophages in MASH liver

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EGR2 is upregulated in monocyte-derived macrophages in MASH liver

Project description:This analysis was perfomed to explore the transcription factors that were enhanced in MASH liver macrophages.

2024-05-02 | GSE263973 | GEO

Lipid Associated Macrophages' Promotion of Fibrosis Resolution during MASH regression requires TREM2

Project description:While macrophage heterogeneity during Metabolic dysfunction-associated steatohepatitis (MASH) has been described, the fate of these macrophages during MASH regression is poorly understood. Comparing macrophage heterogeneity during MASH progression vs regression, we identified specific macrophage sub- populations that are critical for MASH/fibrosis resolution. We elucidated the restorative pathways and gene signatures that define regression associated macrophages (RAM) and establish the importance of TREM2+ macrophages during MASH regression. Liver resident Kupffer cells are lost during MASH and are replaced by four distinct monocyte derived macrophage sub-populations. Trem2 is expressed in two macrophage sub- populations: (i) monocyte-derived macrophages occupying the Kupffer cell niche (MoKC) and (ii) lipid-associated macrophages (LAM). In regression livers, no new transcriptionally distinct MF sub-population emerged. However, the relative macrophage composition changed during regression compared to MASH. While MoKC was the major macrophage sub-population during MASH, they decreased during regression. LAM was the dominant macrophage sub-type during MASH regression and maintained Trem2 expression. Both MoKC and LAM were enriched in disease resolving pathways. Absence of TREM2 restricted the emergence of LAMs and formation of hepatic crown like structures (hCLS). TREM2+ macrophages are functionally important not only for restricting MASH-fibrosis progression, but also for effective regression of inflammation and fibrosis. TREM2+ MF are superior collagen degraders. Lack of TREM2+ macrophages also prevented elimination of hepatic steatosis and inactivation of HSC during regression, indicating their significance in metabolic co-ordination with other cell- types in the liver. TREM2 imparts this protective effect through multifactorial mechanisms, including improved phagocytosis, lipid-handling and collagen degradation.

2024-08-05 | GSE261829 | GEO

Antigen-driven EGR2 expression is required for exhausted CD8+ T cell stability and maintenance [ATACseq]

Project description:In this study, we examined the role of the transcriptional regulator EGR2 in CD8+ T cell exhaustion during chronic viral infection. Flow cytometric and scRNAseq analysis indicated that EGR2 deficient CD8+ T cells had an abnormal effector-like phenotype. To examine whether this was due to epigenetic alterations, we conducted ATACseq analysis on sorted virus-specific tetramer+ CD8+ T cells isolated at day 20 post-infection with chronic LCMV-Cl13 from either littermate control or EGR2 T cell conditional knock-out mice. The resulting data demonstrated that there were substantial epigenetic changes within EGR2 KO CD8+ T cells, suggesting that EGR2 stabilises the exhausted epigenetic state.

2021-03-02 | GSE153136 | GEO

Pro-inflammatory monocyte phenotype during acute progression of cerebral small vessel disease

Project description:The aetiology of cerebral small vessel disease (SVD) remains elusive, though currently evidence is accumulating that inflammation contributes to its pathophysiology. In this prospective high-frequency imaging study, we showed that the incidence of acute SVD progression coincides with a functional and transcriptional pro-inflammatory monocyte phenotype. To detect SVD progression, individuals with SVD underwent monthly magnetic resonance imaging (MRI) for 10 consecutive months. RNA sequencing revealed a pro-inflammatory monocyte signature with upregulation of the EGR2 gene. Collectively, we showed that individuals with progressive SVD have pro-inflammatory circulating monocytes characterized by an augmented cytokine production capacity and a pro-inflammatory transcriptional signature.

2020-12-09 | GSE162790 | GEO

Antigen-driven EGR2 expression is required for exhausted CD8+ T cell stability and maintenance [RNA-seq II]

Project description:In this study, we examined the role of the transcriptional regulator EGR2 in CD8+ T cell exhaustion during chronic viral infection. Flow cytometric analysis indicated that EGR2 is expressed selectively within the progenitor exhausted subset, however a subpopulation of progenitor exhausted cells did not express in EGR2. To define the differences between the EGR2+ and EGR2- progenitor exhausted cells, GFP+ and GFP- polyclonal progenitor exhausted (ie. CD44int-hiPD-1+Slamf6+Tim3-) CD8+ T cells were sorted from Egr2-GFP reporter mice at day 20 p.i. with chronic LCMV-Cl13, and analysed by RNAseq. The resulting data demonstrated that GFP- progenitor cells have a more differentiated phenotype.

2021-03-02 | GSE152849 | GEO

Antigen-driven EGR2 expression is required for exhausted CD8+ T cell stability and maintenance [scRNAseq]

Project description:In this study, we examined the role of the transcriptional regulator EGR2 in CD8+ T cell exhaustion during chronic viral infection. We conducted scRNAseq analysis on sorted virus-specific tetramer+ CD8+ T cells isolated at day 20 post-infection with chronic LCMV-Cl13 from either littermate control or EGR2 T cell conditional knock-out mice. Cells were labelled with hashtags and mixed prior to multiplexed analysis. The resulting data demonstrated that the exhausted cell subsets within EGR2 KO CD8+ T cells have an effector-like phenotype, suggesting that EGR2 stabilises the exhausted state.

2021-03-02 | GSE154143 | GEO

Antigen-driven EGR2 expression is required for exhausted CD8+ T cell stability and maintenance [CHIP-seq]

Project description:In this study, we examined the role of the transcriptional regulator EGR2 in CD8+ T cell exhaustion during chronic viral infection. Flow cytometric and RNAseq analysis indicated that EGR2 deficient CD8+ T cells had a block in differentiation and failed to undergo terminal exhaustion. To examine the direct gene targets of EGR2 during exhaustion, we conducted ChIPseq analysis on enriched bulk splenic CD8+ T cells isolated at day 20 post-infection with chronic LCMV-Cl13 from C57BL/6J mice. The resulting data demonstrated that EGR2 directly controls expression of key gene targets, including Pdcd1, Tigit, Cxcr5, Tcf7, Bach2 and Bcl6.

2021-03-02 | GSE134708 | GEO

Antigen-driven EGR2 expression is required for exhausted CD8+ T cell stability and maintenance [RNA-seq I]

Project description:In this study, we examined the role of the transcriptional regulator EGR2 in CD8+ T cell exhaustion during chronic viral infection. Flow cytometric analysis indicated that EGR2 deficient CD8+ T cells had a block in differentiation and failed to undergo terminal exhaustion. To confirm this at a whole transcriptome level, we conducted RNAseq analysis on sorted splenic virus-specific tetramer+ CD8+ T cells isolated at day 20 post-infection with chronic LCMV-Cl13 from either littermate control or EGR2 T cell conditional knock-out mice. The resulting data demonstrated that there was a global loss of the terminally exhausted gene signature within EGR2 KO CD8+ T cells. This suggests that EGR2 promotes terminal CD8+ T cell exhaustion.

2021-03-02 | GSE134689 | GEO

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