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TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration

ABSTRACT: TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration

PROVIDER: PRJNA875133 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21356437_1.fastq.gz	Fastqsanger.gz
	SRR21356437_2.fastq.gz	Fastqsanger.gz
	SRR21356438_1.fastq.gz	Fastqsanger.gz
	SRR21356438_2.fastq.gz	Fastqsanger.gz
	SRR21356439_1.fastq.gz	Fastqsanger.gz

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TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (scRNA-Seq)

Project description:TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (scRNA-Seq)

| PRJNA875139 | ENA

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (RNA-Seq)

Project description:TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (RNA-Seq)

| PRJNA875138 | ENA

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (RNA-Seq)

Project description:IFNγ is traditionally known as a pro-inflammatory cytokine with diverse roles in antimicrobial and antitumor immunity. Yet, findings regarding its sources and functions during the regeneration process following a sterile injury are conflicting. Here, we show that natural killer (NK) cells are the main source of IFNγ in regenerating muscle. Beyond this cell population, IFNγ production is limited to a small population of T cells. We further show that NK cells do not play a major role in muscle regeneration following an acute injury or in dystrophic mice. Surprisingly, the absence of IFNγ per se also has no effect on muscle regeneration following an acute injury. However, the role of IFNγ is partially unmasked when TNFα is also neutralized, suggesting a compensatory mechanism. Using transgenic mice, we showed that conditional inhibition of IFNGR1 signaling in muscle stem cells or fibro-adipogenic progenitors does not play a major role in muscle regeneration. In contrast to common belief, we found that IFNγ is not present in the early inflammatory phase of the regeneration process, but rather peaks when macrophages are acquiring an anti-inflammatory phenotype. Our further transcriptomic analysis suggests that IFNγ cooperates with TNFα to regulate the transition of macrophages from pro- to anti-inflammatory. The absence of the cooperative effect of these cytokines on macrophages, however, does not result in significant regeneration impairment likely due to the presence of other compensatory mechanisms. Our findings support the arising view of IFNγ as a pleiotropic inflammatory regulator rather than an inducer of the inflammatory response.

2022-10-25 | GSE212372 | GEO

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (scRNA-Seq)

2022-10-25 | GSE212371 | GEO

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration.

Project description: Not available

| S-EPMC9636974 | biostudies-literature

Mouse trophoblast cells have attenuated responses to TNFα and IFNγ that allow them to avoid synergic cytotoxicity of the two cytokines

Project description:TNFα and IFNg are two inflammatory cytokines that play critical roles in immune responses, but they can also negatively affect cell proliferation and viability. In particular, the combination of the two cytokines (TNFα/IFNγ) synergistically causes death in many cell types. We recently demonstrated that, mouse embryonic stem cells (ESCs) isolated from the inner cell mass of the blastocyst stage embryo, do not respond to TNFα and IFNg, thereby avoiding TNFα/IFNγ cytotoxicity. This study expanded our investigation to mouse trophoblast stem cells (TSCs) and differentiated trophoblasts (TSC-TBs), the major cellular constituents in trophectoderm of the blastocyst. We report here that TNFα or IFNγ alone has limited negative effect on the viability of mouse fibroblasts, but TNFα/IFNγ effectively kill these cells. However, TSCs and TSC-TBs are markedly resistant to the cytotoxicity of TNFα/IFNγ. With molecular and cellular approaches and transcriptomic analysis, we demonstrated that TSCs and TSC-TBs have attenuated responses to TNFα and IFNγ and the underlying molecular mechanisms that allow these cells to avoid the synergistic cytotoxicity of TNFα/IFNγ. Together with our previous findings in ESCs, we propose that the attenuated responses of TSCs, TSC-TBs, and ESCs to TNFα and IFNγ may serve as a protective mechanism that limits cytokine cytotoxicity in the blastocyst.

2023-11-10 | GSE224755 | GEO

Transcriptomic profiling of human RPTECs following TNFα and IFNγ stimulation at early and late time points

Project description:Renal proximal tubule epithelial cells (RPTECs) were stimulated with TNFα, IFNγ, or a combination of TNFα and IFNγ to characterize cytokine-induced transcriptional responses. Bulk RNA sequencing was performed at 3 h and 12 h following treatment to capture early and sustained gene expression changes. This dataset enables analysis of inflammatory signaling dynamics and cytokine-specific versus cooperative transcriptional programs in human tubular epithelial cells

2026-06-16 | GSE319877 | GEO

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration

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

2022-10-25 | GSE212373 | GEO

CUT&RUN profiling of ELF3 and NFKB2 binding landscapes in primary mouse tubular epithelial cells under TNFα and IFNγ stimulation

Project description:Primary mouse renal tubular epithelial cells were cultured and stimulated with TNFα and IFNγ to model inflammatory activation. CUT&RUN assays were performed using antibodies targeting ELF3, NFKB2, and IgG control to define genome-wide chromatin binding profiles. This dataset enables characterization of ELF3- and NFKB2-associated regulatory regions in cytokine-stimulated tubular epithelial cells.

2026-06-16 | GSE319848 | GEO

MiR-155 promotes blood-brain barrier dysfunction in neuroinflammation (part 1)

Project description:Here, we investigated the time-course changes in the pattern of microRNA (miRNA) expression of TNFα and IFNγ-stimulated and unstimulated hCMEC/D3 cells, an immortalized human cerebral microvascular endothelial cell line. In order to investigate pro-inflammatory cytokine-induced changes in miRNA levels in hCMEC/D3 cells, we challenged brain endothelial cells with TNFα and IFNγ (100 ng/ml) for 2 h, 6 h and 24 h and determined microRNA expression in cytokine-stimulated and unstimulated cells

2014-04-29 | E-GEOD-44692 | biostudies-arrayexpress

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