Bulk RNA-sequencing of human non-IBD enteroids treated with interferon-gamma (IFNγ)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1227985 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the intestinal epithelial cellular responses to interferon-gamma (IFNγ), bulk RNA sequencing (RNA-seq) was performed on human small intestinal organoids (enteroids, n = 6) with and without IFNγ treatment (100 pg/ml). The enteroids were derived from endoscopic biopsy samples obtained from patients without inflammatory bowel disease (IBD).
2025-03-15 | GSE290418 | GEO
Project description:To investigate the intestinal epithelial cellular responses to interferon-gamma (IFNγ), bulk RNA sequencing (RNA-seq) was performed on human small intestinal organoids (enteroids, n = 10) with and without IFNγ treatment (100 pg/ml). The enteroids were derived from endoscopic biopsy samples obtained from patients with Crohn's disease (CD).
2025-03-15 | GSE290417 | GEO
Project description:Bulk RNA-sequencing of human Crohn's disease (CD) enteroids treated with interferon-gamma (IFNγ)
| PRJNA1227986 | ENA
Project description:Rateitschak2012 - Interferon-gamma (IFNγ) induced STAT1 signalling (PC_IFNg100)
This model is described in the article:
Parameter identifiability and sensitivity analysis predict targets for enhancement of STAT1 activity in pancreatic cancer and stellate cells.
Rateitschak K, Winter F, Lange F, Jaster R, Wolkenhauer O.
PLoS Comput. Biol. 2012; 8(12): e1002815
Abstract:
The present work exemplifies how parameter identifiability analysis can be used to gain insights into differences in experimental systems and how uncertainty in parameter estimates can be handled. The case study, presented here, investigates interferon-gamma (IFNγ) induced STAT1 signalling in two cell types that play a key role in pancreatic cancer development: pancreatic stellate and cancer cells. IFNγ inhibits the growth for both types of cells and may be prototypic of agents that simultaneously hit cancer and stroma cells. We combined time-course experiments with mathematical modelling to focus on the common situation in which variations between profiles of experimental time series, from different cell types, are observed. To understand how biochemical reactions are causing the observed variations, we performed a parameter identifiability analysis. We successfully identified reactions that differ in pancreatic stellate cells and cancer cells, by comparing confidence intervals of parameter value estimates and the variability of model trajectories. Our analysis shows that useful information can also be obtained from nonidentifiable parameters. For the prediction of potential therapeutic targets we studied the consequences of uncertainty in the values of identifiable and nonidentifiable parameters. Interestingly, the sensitivity of model variables is robust against parameter variations and against differences between IFNγ induced STAT1 signalling in pancreatic stellate and cancer cells. This provides the basis for a prediction of therapeutic targets that are valid for both cell types.
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2024-09-02 | BIOMD0000000585 | BioModels
Project description:Interferon-gamma (IFNγ) is a critical cytokine required to coordinate anti-viral immunity in response to pathogens such as influenza. IFNγ signals through the JAK-STAT pathway, inducing a tyrosine-phosphorylation cascade that ensures a potent immune response. Aberrant JAK-STAT signaling can drive hyperinflammation and autoimmunity, and thus signaling is tightly and selectively regulated by the IFNγ-inducible protein, Suppressor of Cytokine Signaling 1 (SOCS1). SOCS1 inhibits signaling by directly blocking JAK kinase activity. Here we identified a SOCS1-interacting partner, ARAP2 that fine-tunes SOCS1 function. We report that tyrosine 415 in ARAP2 binds the SOCS1-Src Homology 2 (SH2) domain and limits the ability of SOCS1 to inhibit IFNγ signaling. Our findings reveal ARAP2 as a key player in influenza immunity that promotes the IFNγ response through a phosphorylation dependent interaction with the negative regulator SOCS1.
2025-10-06 | PXD060300 | Pride
Project description:RNA-seq analysis of murine microglial BV2 cells treated with interferon-gamma (IFNγ)
| PRJNA548876 | ENA
Project description:Episodic Ebola virus (EBOV) outbreaks, such as the current one in West Africa, emphasize the critical need for novel antivirals against this highly pathogenic virus. Here, we demonstrate that interferon gamma (IFNγ) prevents morbidity and mortality associated with EBOV infection when administered to mice either 24 hours prior to or 2 hours following EBOV infection. Microarray studies with IFNγ-stimulated human macrophages identified novel interferon-stimulated genes (ISGs) that inhibit EBOV infection upon ectopic expression. IFNγ treatment reduced viral RNA levels in macrophages to a similar degree as cells treated with the protein synthesis inhibitor, cycloheximide, suggesting that IFNγ treatment inhibits genome replication. As IFNγ treatment robustly protects mice against EBOV infection, we propose that this FDA-approved drug may serve as a useful prophylactic or therapeutic strategy during EBOV outbreaks, contributing to the currently limited arsenal of filovirus antivirals.
2015-10-20 | GSE64995 | GEO
Project description:Episodic Ebola virus (EBOV) outbreaks, such as the current one in West Africa, emphasize the critical need for novel antivirals against this highly pathogenic virus. Here, we demonstrate that interferon gamma (IFNγ) prevents morbidity and mortality associated with EBOV infection when administered to mice either 24 hours prior to or 2 hours following EBOV infection. Microarray studies with IFNγ-stimulated human macrophages identified novel interferon-stimulated genes (ISGs) that inhibit EBOV infection upon ectopic expression. IFNγ treatment reduced viral RNA levels in macrophages to a similar degree as cells treated with the protein synthesis inhibitor, cycloheximide, suggesting that IFNγ treatment inhibits genome replication. As IFNγ treatment robustly protects mice against EBOV infection, we propose that this FDA-approved drug may serve as a useful prophylactic or therapeutic strategy during EBOV outbreaks, contributing to the currently limited arsenal of filovirus antivirals.
2015-10-20 | GSE64996 | GEO
Project description:There is limited understanding of how immune-mediated damage impacts intestinal stem cells (ISCs). We found that stem cell compartment injury is a shared feature of both alloreactive and autoreactive intestinal immunopathology, reducing ISCs and impairing their recovery in T-cell-mediated injury models. Modeling with ex vivo epithelial cultures indicated ISC depletion and impaired human as well as murine organoid survival upon co-culture with activated T cells, and screening of effector pathways identified Interferon-γ (IFNγ) as a principal mediator of ISC compartment damage. Flow cytometry analysis confirmed expression of IFNγ receptor on ISCs. To investigate if the receptor was functional, we performed transcriptome analysis of ISCs treated with IFNγ. In brief, mRNA profiles of sorted Lgr5-high cells treated with/without IFNγ were generated by deep sequencing, in triplicate, using the TruSeq SBS Kit V4 (Illumina). RNA profiles confirmed a robust IFNγ transcriptional signature in the stem cells, as several IFNγ-related genes were upregulated shortly after exposure, indicating direct activity of IFNγ in ISCs. Epithelial cultures with IFNγ-receptor-deficient ISCs and purified stem cell colonies also indicated direct targeting of the ISCs. This study showed that dysregulated T cell activation and Interferon-γ production are potent mediators of ISC injury.
2019-11-02 | GSE139813 | GEO
Project description:This experiment tested whether pretreatment of human microvascular endothelial cells (HMECs) with interferon-gamma (IFNγ) for 2h affected the transcriptional response to 1h exposure to interleukin-6 (IL-6).
2009-11-19 | GSE19082 | GEO