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Negative feedback of IFN-I signaling through IFN-competent RIG-I-like receptor-induced HSPA6

ABSTRACT: Negative feedback of IFN-I signaling through IFN-competent RIG-I-like receptor-induced HSPA6

PROVIDER: PRJNA1057862 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27368470_1.fastq.gz	Fastqsanger.gz
	SRR27368470_2.fastq.gz	Fastqsanger.gz
	SRR27368471_1.fastq.gz	Fastqsanger.gz
	SRR27368471_2.fastq.gz	Fastqsanger.gz
	SRR27368472_1.fastq.gz	Fastqsanger.gz

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Negative feedback of IFN-I signaling through IFN-competent RIG-I-like receptor-induced HSPA6

Project description:The RIG-I-like receptors (RLRs) form filaments to activate type-I interferon (IFN-I) and NF-KB signaling through their adaptor protein MAVS and downstream cascades. These filaments are recognized and regulated by cell-encoded machinery for correct activation. Here, we identified the stress-sensitive heat shock protein, HSPA6, was induced to express upon RLR-MAVS activation to act as a negative regulator of IFN-I signaling. Interestingly, by using MAVS-KO cells, we showed that HSPA6 was upregulated dependent on the presence of IFN-competent RLRs but not MAVS. Gene knockout (KO) tests indicated that the E3 ligases, stress granules (SGs), and transcription factors IRF1 and AP1 were all shared to induce HSPA6 and the canonical IFNb. Kinetic analysis showed that HSPA6 upregulated slower than IFNb, implicating these two genes competed machinery for transcription activation. Further tests suggested the induced HSPA6 bound to IFN-competent MDA5 to dissolve the filaments and downregulated IFN induction. Thus, our study uncovered a new gene activation mechanism by the IFN-competent RLRs to serve as negative feedback, arguing for a gene regulatory role of functional filaments of innate immunity.

2024-01-01 | GSE252140 | GEO

IFN-mediated negative feedback supports bacteria class-specific macrophage inflammatory responses

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Type I IFN-signaling following Pneumocystis (PC)-infection and clearance in CD4 T cell-competent mice

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Type I IFN-signaling following Pneumocystis (PC)-infection and clearance in CD4 T cell-competent mice

Project description:Type I IFN-signaling suppresses an excessive IFN-{gamma} response and prevents lung damage and chronic inflammation following Pneumocystis (PC)-infection and clearance in CD4 T cell-competent mice. Type I IFN -signaling in pulmonary CD11c+ DCs and alveolar macrophages may prevent chronic inflammation following PC lung infection and clearance by suppressing an excessive IFN-g-response via the induction of SOCS1. IFNAR-/- and wildtype mice were both Pneumocystis infected via itratracheal instillation. Pulmonary CD11c+ cells were isolated from collagen digested lungs at day 7 and day 14 post infection from both wildtype and IFNAR-/- mice using a magnetic cell sorting technique from Miltenyi with CD11c microbeads. Cells from three individual animals per group were isolated and assessed. Comparison of 2 treatment types at 2 timepoints to determine whether type I IFN signaling is initiated in resident and early recruited pulmonary CD11c+ cells following Pneumocystis lung infection and whether this is relevant to the outcome of the inflammatory response during the initiation of clearance.

2010-07-07 | E-GEOD-18607 | biostudies-arrayexpress

Negative Feedback Regulation of Cholesterol Biosynthesis by MMAB

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Interferon regulated genes in mouse intestine after irradiation and prophylactic Rig-I activation

Project description:As RIG-I activation induces potent IFN-I responses,we analyzed the role of IFN-I in intestinal tissue protection and prevention of GVHD. We performed RNA sequencing with tissue samples from SI of WT mice that received TBI -/+ previous 3pRNA treatment and -/+ antibody-mediated blockade of IFNAR. Application of 3pRNA before TBI resulted in a significant increase of IFN-inducible genes in the SI as compared to solely irradiated mice. Blockade of IFNAR signaling abrogated 3pRNA-mediated up-regulation of IFN-induced genes, demonstrating that RIG-I-induced gene-regulation depends on IFN-I.

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A stimulus-contingent positive feedback loop enables IFN-β dose-dependent activation of pro-inflammatory genes

Project description:Type I interferons (IFN) induce powerful anti-viral and innate immune responses via the transcription factor, IFN-stimulated gene factor (ISGF3). However, in some pathological contexts type I IFNs are responsible for exacerbating inflammation. Here, we show that a high dose of IFN-β also activates an inflammatory gene expression program in contrast to IFN-λ3, a type III IFN, which elicits only the common anti-viral gene program. We show that the inflammatory gene program depends on a second, potentiated phase in ISGF3 activation. Iterating between mathematical modeling and experimental analysis we show that the ISGF3 activation network may engage a positive feedback loop with its subunits IRF9 and STAT2. This network motif mediates stimulus-specific ISGF3 dynamics that are dependent on ligand, dose, and duration of exposure, and when engaged activates the inflammatory gene expression program. Our results reveal a previously underappreciated dynamical control of the JAK-STAT/IRF signaling network that may produce distinct biological responses, and suggest that studies of type I IFN dysregulation, and in turn therapeutic remedies, may focus on feedback regulators within it.

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