Cell specific response to IFNg
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE112876
PROVIDER: PRJNA449370 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report cell specific responses to IFNg in 11 different peripheral immunocyte populations in the mouse. These cells represent the core ImmGen immunocyte lineage panel. Profiles from these were used to analyze cell specific responses to IFNg. In general a core set of ISG transcripts are induced in all cells. Smaller sets of ISGs were induced in a cell specific manner. In particular, splenic granulocytes and dendritic cells show restriced indcution of sets of ISGs.
2018-04-10 | GSE112876 | GEO
Project description:We seeked to determine in vivo effects of IFNg and IFNa response in peritoneal cavity macrophages. These cells were part of ImmGen Interferon cytokine study and immunocytes were sorted according to Immgen's standard lineage panel. Profiles from peritoneal cavity macrophages were used to analyze cell specific responses to IFNg.
2018-02-14 | GSE110549 | GEO
Project description:Interferon gamma (IFNg) is a pivotal cytokine that activates macrophages and shapes their response to subsequent inflammatory stimuli. Here, we investigated the distinct roles of STAT1 isoforms, STAT1alpha and STAT1beta, in IFNg-induced epigenetic remodelling and subsequent responses to lipopolysaccharide (LPS) in primary macrophages. We show that the STAT1 C-terminal TAD, which is missing in the STAT1beta isoform, is required for both H3K27 acetylation and deacetylation in response to IFNg. Notably, H3K27 deacetylation was associated with AP-1 motifs rather than STAT1 binding, suggesting indirect regulatory mechanisms. Functionally, IFNg pretreatment suppressed the induction of anti-inflammatory and virus response genes, including a subset of IFN-stimulated genes (ISGs), in response to LPS, while enhancing the expression of a distinct set of ISGs. Mechanistically, the STAT1 C-terminal TAD was critical for IFNg-mediated inhibition of LPS-induced enhancer activation at key regulatory genes, such as Il10 and Irak3, which are involved in negative feedback of toll-like receptor (TLR) signalling. Conversely, cooperative gene activation by IFNg and LPS was largely independent of the STAT1 C-terminal TAD, with notable exceptions, such as Ido1 and Tgtp1. Genome-wide analysis indicated that IRF1 and IRF8, rather than STAT1 homodimers, predominantly mediate in IFNg-induced H3K27 acetylation and transcription factor network analysis identified additional regulators integrating IFNg and LPS responses. Together, these findings reveal gene- and isoform-specific roles of STAT1 in coordinating IFNg-dependent chromatin remodelling and transcriptional cross-regulation, providing new insights into the control of inflammation and innate immunity.
2025-09-30 | GSE309503 | GEO
Project description:NGS5522 - hMDMS response to IFNg and TNFa
| PRJNA1116550 | ENA
Project description:We did transcriptome profiling for monocytes treated with or without IFNg to characterize IFNg response.
2016-09-12 | GSE84691 | GEO
Project description:Peritoneal cavity macrophage response to IFNg and IFNa
| PRJNA433974 | ENA
Project description:Interferon gamma (IFNg) is a pivotal cytokine that activates macrophages and shapes their response to subsequent inflammatory stimuli. Here, we investigated the distinct roles of STAT1 isoforms, STAT1alpha and STAT1beta, in IFNg-induced epigenetic remodelling and subsequent responses to lipopolysaccharide (LPS) in primary macrophages. We show that the STAT1 C-terminal TAD, which is missing in the STAT1beta isoform, is required for both H3K27 acetylation and deacetylation in response to IFNg. Notably, H3K27 deacetylation was associated with AP-1 motifs rather than STAT1 binding, suggesting indirect regulatory mechanisms. Functionally, IFNg pretreatment suppressed the induction of anti-inflammatory and virus response genes, including a subset of IFN-stimulated genes (ISGs), in response to LPS, while enhancing the expression of a distinct set of ISGs. Mechanistically, the STAT1 C-terminal TAD was critical for IFNg-mediated inhibition of LPS-induced enhancer activation at key regulatory genes, such as Il10 and Irak3, which are involved in negative feedback of toll-like receptor (TLR) signalling. Conversely, cooperative gene activation by IFNg and LPS was largely independent of the STAT1 C-terminal TAD, with notable exceptions, such as Ido1 and Tgtp1. Genome-wide analysis indicated that IRF1 and IRF8, rather than STAT1 homodimers, predominantly mediate in IFNg-induced H3K27 acetylation and transcription factor network analysis identified additional regulators integrating IFNg and LPS responses. Together, these findings reveal gene- and isoform-specific roles of STAT1 in coordinating IFNg-dependent chromatin remodelling and transcriptional cross-regulation, providing new insights into the control of inflammation and innate immunity.
2025-09-30 | GSE309564 | GEO
Project description:Gene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood Ex vivo sorted Tregs (CD25highCD127neg) were stimulated for 4 hours and IFNg-secreting cells were detected by a IFNg-capture kit. The samples were resorted based on IFNg expression.
2016-07-01 | E-GEOD-71274 | biostudies-arrayexpress
Project description:human primay macrophages (hMDMs) were unstimulated, stimulated with IFNg or costimulated with IFNg and TNFa for 18h
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Project description:Gene expression studies comparing IFNg+ Tregs versus IFNg- Tregs from human peripheral blood
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