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Effect of JAK-JAK Geometry on Gene Expression Levels in Cells Treated with Type I and III Interferons

ABSTRACT: Effect of JAK-JAK Geometry on Gene Expression Levels in Cells Treated with Type I and III Interferons

PROVIDER: PRJNA859134 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20230839.fastq.gz	Fastqsanger.gz
	SRR20230840.fastq.gz	Fastqsanger.gz
	SRR20230841.fastq.gz	Fastqsanger.gz
	SRR20230842.fastq.gz	Fastqsanger.gz
	SRR20230843.fastq.gz	Fastqsanger.gz

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Effect of JAK-JAK Geometry on Gene Expression Levels in Cells Treated with Type I and III Interferons

Project description:To evaluate the role of receptor geometry in interferon signaling, we engineered cell lines that express wild-type and mutant IFNλ cognate receptors (IFNλR1) with rotated intracellular registers with respect to the associated JAK1. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cell lines treated with 3 indicated interferons at 24hr.

2024-07-01 | GSE208288 | GEO

Type III interferons induce pyroptosis in gut epithelial cells and impair tissue repair upon intestinal injury.

Project description:Tissue damage and repair are hallmarks of inflammation. Despite a wealth of information on the mechanisms that govern tissue damage, mechanistic insight on how inflammation affects repair is lacking. Here, we investigated how interferons influence tissue repair after damage to the intestinal mucosa. We found that type III, not type I or II, interferons delay epithelial cell regeneration by inducing the upregulation of Z-DNA-binding protein 1 (ZBP1). Z-nucleic acids formed following intestinal damage are sensed by ZBP1, leading to Caspase-8 activation, and cleavage of Gasdermin C (GSDMC). Cleaved GSDMC drives epithelial cell death by pyroptosis and delays repair of the large or small intestine after colitis or irradiation, respectively. The type III interferon/ZBP1/Caspase-8/GSDMC axis is also active in patients with inflammatory bowel disease (IBD). Our findings highlight the capacity of type III interferons to delay gut repair, which has important implications for IBD patients or individuals exposed to radiation therapies.

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Type III interferons induce pyroptosis in gut epithelial cells and impair tissue repair upon intestinal injury.

Project description:Tissue damage and repair are hallmarks of the inflammatory process. Despite a wealth of information on the mechanisms that govern tissue damage, mechanistic insight on how inflammatory mediators affect repair is lacking. Here, we investigated how interferons influence tissue repair after damage to the intestinal mucosa driven by inflammation or genotoxicity. We found that type III, but not type I or II, interferons delay epithelial cell regeneration by inducing the upregulation of Z-DNA-binding protein 1 (ZBP1). Z-nucleic acids formed during the damage and repair process are then sensed by ZBP-1, leading to Caspase-8 activation, and cleavage of Gasdermin C (GSDMC). Cleaved GSDMC drives epithelial cell death by pyroptosis and delays the re-epithelialization of the large or small intestine after colitis or irradiation, respectively. We also found that the type III interferon/ZBP1/Caspase-8/GSDMC pathway is activated in patients with inflammatory bowel disease (IBD). Our findings highlight a molecular signaling cascade initiated by type III interferons that delays intestinal tissue repair, which has important implications for IBD patients or individuals exposed to radiation therapies.

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Distinct immune responses to type I and III interferons are regulated by interferon regulatory factor 1

Project description:Type I and III interferons (IFNs) are critical antiviral molecules thought to activate similar signaling cascades resulting in the induction of shared downstream IFN-stimulated genes. This study reveals an unappreciated fundamental difference in the signal transduction downstream of type I and type III IFNs that has broad implications for their functionalities during infection and inflammation.

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Type III interferons induce pyroptosis in gut epithelial cells and delay tissue restitution upon intestinal injury

Project description:To investigate the transcriptional program within the intestinal epithelial cells (IECs) controlling the impact of type III interferons (IFN-λ) on intestinal recovery, we performed a single-cell RNA sequencing (scRNA-seq) on murine IECs following irradiation.

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Eutherian interferons

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Transcription profiling by array of primary human hepatocytes derived from hepatitis C patients treated with type III interferons (IFNs) for 6 or 24 hours

Project description:Recent identification of IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III interferons (IFNs) in hepatitis C infection. The function of type III IFNs in intrinsic antiviral immunity is poorly understood. Here we show that HCV infection of primary human hepatocytes results in a robust induction of type III but not type I IFNs, leading to IFN- stimulated gene (ISG) expression. In addition, HCV infection elicits a much broader range of gene expression alterations in addition to ISG induction. The induction of type III IFNs is mediated by IRF3 and NFkB- dependent pathways. Type III IFN, aside from upregulating ISGs with a different kinetic profile, induces a distinct set of genes from type I IFN, potentially explaining the functional difference between the two types of IFNs. Chimpanzees undergoing experimental HCV infection demonstrated a prompt hepatic induction of IL28, associating with ISG upregulation, but minimal type I IFN induction. Analysis of liver biopsies from HCV-infected patients supported a close correlation among hepatic expression of IL28 and ISGs, but not with type I IFNs. Our study demonstrates that HCV infection results predominantly in type III IFN induction in the liver and the level of induction correlates with hepatic ISG levels, thus providing a mechanistic explanation for the association between IL28, ISG levels and recovery from HCV infection as well as a potential therapeutic strategy for the treatment of non-responders. Samples were treated with IFN or IL28b after 6 or 24 hours with three replications

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Effect of JAK blockade on IFNa response in B cells in vitro

Project description:B cells respond robustly to type 1 interferons which signal through JAK1 and TYK2. Here we analyzed the effects of a panel of JAK inhibitors on the IFNa transcriptional response in activated B cells in vitro. Splenic B cells were isolated by negative selection from 6wk old male C57BL/6 mice. These were activated with LPS(10ug/ml) for 48hrs and thereafter cultured with IFNa (100U/ml) in the presence or absence of JAK inhibitors at IC80 for 2hrs or 8hrs in vitro. Cells were then transferred directly into TriZol. RNA was prepared in Trizol for gene expression profiling by Affymetrix Mouse Gene 1.0 ST Arrays.

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Antiviral function of type I and type III interferons in the olfactory epithelium

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