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CD4+ T cells select unique P65, IRF1 and FOS dependen responses in APC for integration into antiviral CD8+ T cell immunity

ABSTRACT: CD4+ T cells select unique P65, IRF1 and FOS dependen responses in APC for integration into antiviral CD8+ T cell immunity

PROVIDER: PRJNA942315 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23752900_1.fastq.gz	Fastqsanger.gz
	SRR23752900_2.fastq.gz	Fastqsanger.gz
	SRR23752901_1.fastq.gz	Fastqsanger.gz
	SRR23752901_2.fastq.gz	Fastqsanger.gz
	SRR23752902_1.fastq.gz	Fastqsanger.gz

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CD4+ T cells select unique P65, IRF1 and FOS dependen responses in APC for integration into antiviral CD8+ T cell immunity

Project description:Antiviral CD8+ T cell immunity depends on the integration of varying contextual cues, but how antigen presenting cells (APC ) consolidate these signals for decoding by T cells remains unclear. We describe gradual IFN-α/β-induced transcriptional adaptations that endowed APC with the capacity to rapidly activate the transcriptional regulators P65, IRF1 and FOS upon CD4+ T cell-mediated CD40 stimulation. While these responses operated through broadly utilized signaling components, they induced a unique set of costimulatory molecules and soluble mediators that could not be elicited by IFN-α/β or CD40 alone. This response was critical for the acquisition of antiviral CD8+ T cell effector function, and its activity in APC from patients infected with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) correlated with milder disease. These observations uncover a sequential integration process whereby APC rely on CD4+ T cells to select the innate circuits that guide antiviral CD8+ T cell responses.

2024-02-20 | GSE226959 | GEO

p65

Project description:p65

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Investigating the role of YAP and FOS in driving OnF reporgramming during tumor intiation

Project description:To investigate the role of YAP and FOS in early OnF reporgramming, we knocked down either gene during tumor intiation induced by APC depletion.

2024-10-17 | GSE263047 | GEO

Relief of extracellular matrix deposition repression by downregulation of IRF1-mediated TWEAK/Fn14 signaling in keloids

Project description:Keloids represent a fibrotic disorder characterized by the excessive deposition of extracellular matrix (ECM). However, the mechanisms by which ECM deposition in keloids is regulated remain elusive. Here, we found that the expression of both TWEAK and its cognate receptor Fn14 was significantly downregulated in keloids and that TWEAK/Fn14 signaling repressed the expression of ECM-related genes in keloid fibroblasts. The IRF1 gene was essential for this repression, and the TWEAK/Fn14 downstream transcription factor P65 directly bound to the promoter of the IRF1 gene and induced its expression. Furthermore, in keloid patients, the expression of TWEAK and Fn14 was negatively correlated with that of ECM genes and positively correlated with that of IRF1. These observations indicate that relief of TWEAK/Fn14/IRF1-mediated ECM deposition repression contributes to keloid pathogenesis, and the identified mechanism and related molecules provide potential targets for keloid treatment in the future.

2023-01-28 | GSE221382 | GEO

Oncogenic Ras inhibits IRF1 to promote viral oncolysis

Project description:Oncolytic viruses exploit common molecular changes in cancer cells, which are not present in normal cells, to target and kill cancer cells. Ras transformation and defects in type I interferon (IFN)-mediated antiviral responses are known to be the major mechanisms underlying viral oncolysis. Previously, we demonstrated that oncogenic RAS/Mitogen-activated protein kinase kinase (Ras/MEK) activation suppresses the transcription of many IFN-inducible genes in human cancer cells, suggesting that Ras transformation underlies type I IFN defects in cancer cells. Here, we investigated how Ras/MEK downregulates IFN-induced transcription. By conducting promoter deletion analysis of IFN-inducible genes, namely guanylate-binding protein 2 and IFN gamma inducible protein 47 (Ifi47), we identified the IFN regulatory factor 1 (IRF1) binding site as the promoter region responsible for the regulation of transcription by MEK. MEK inhibition promoted transcription of the IFN-inducible genes in wild type mouse embryonic fibroblasts (MEFs), but not in IRF1?/? MEFs, showing that IRF1 is involved in MEK-mediated downregulation of IFN-inducible genes. Furthermore, IRF1 protein expression was lower in RasV12 cells compared with vector control NIH3T3 cells, but was restored to equivalent levels by inhibition of MEK. Similarly, the restoration of IRF1 expression by MEK inhibition was observed in human cancer cells. IRF1 re-expression in human cancer cells caused cells to become resistant to infection by the oncolytic vesicular stomatitis virus strain. Together, this work demonstrates that Ras/MEK activation in cancer cells downregulates transcription of IFN-inducible genes by targeting IRF1 expression, resulting in increased susceptibility to viral oncolysis. RNA was isolated from RasV12 transformed NIH/3T3 cells (RasV12 cells) treated with 20?M U0126 or 500U/ml IFN-?, or left untreated, for 6 hours, triplicate biological samples (9 samples).

2014-11-13 | E-GEOD-49469 | biostudies-arrayexpress

IRF1 mass-spectrometry primary fibroblasts non-stimulated or stimulated with IFNg for 24h

Project description:Inborn errors of human IFN-γ immunity underlie mycobacterial diseases, whereas inborn errors of IFN-a/b immunity underlie viral diseases. Both types of IFNs induce the transcription factor IRF1. We describe two unrelated children with inherited complete IRF1 deficiency and early-onset, multiple, life-threatening diseases caused by weakly virulent mycobacteria. These children have no history of severe viral disease, despite exposure to many viruses, including SARS-CoV-2, which is life-threatening in individuals with impaired IFN-a/b immunity. The IRF1-dependent cellular responses to IFN-γ are, both quantitatively and qualitatively, much greater than those to IFN-a/b in vitro. Monocyte- and iPSC-derived macrophages from the two patients show no upregulation of at least 20% of the target genes normally induced by IFN-γ. By contrast, cell-intrinsic IFN-a/b immunity to diverse viruses, including SARS-CoV-2, is intact. Human IRF1 is, thus, largely redundant for antiviral IFN-a/b immunity. By contrast, human IRF1 is essential for IFN-γ immunity to mycobacteria in myeloid cells.

2023-01-19 | PXD037759 | Pride

Effects of p65 palmitoylation on gene expression when overexpressing vector or p65 WT or p65 2CS in p65 knockout 293A cells combined with TNFα treatment

Project description:Nuclear factor kappa B (NF-κB) is a central regulator of inflammation, infection, and immunity pathways and is often dysregulated in autoimmune diseases, inflammatory disorders, and cancers. However, the mechanisms by which different stimuli, including cellular metabolism, modulate NF-κB activation remain unclear. Here, we report that RelA ( p65), a major component of NF-κB, is S-palmitoylated at cysteine 197 and 206 by directly reacting with palmitoyl-CoA. Autopalmitoylation of p65 promotes its nuclear localization and p65-p50 complex formation, thereby enhancing NF-κB transcriptional activities. Furthermore, p65 palmitoylation upregulates RelB expression and promotes non-canonical NF-κB complex formation, further amplifying pathway activation. We also demonstrate that a high-fat diet could enhance p65 palmitoylation and correlate with an increased cytokine production in mouse tissues. These results reveal that lipid metabolism might directly regulate NF-κB activity and suggest that targeting p65 auto-palmitoylation could be a potential therapeutic strategy for diseases with deregulated NF-κB pathway.

2025-01-17 | GSE286561 | GEO

p65-HaloTag copurifying proteins in human 293T cells

Project description:In effort to develop methodology for targeted top down mass spectrometry of NF kappa B p65 from human cells, we evaluated the utility of HaloTag for purification and analysis of recombinant protein. During our study, two datasets of bottom up LC-MS/MS were generated: one from in-gel digestion of the predominant band following p65-HaloTag purification, another from in-solution digestion of all the proteins present in a p65-HaloTag purification. p65-HaloTag copurifying proteins identified in our datasets include the known interactors c-Rel, NF-kappaB p105, NF-kappaB p100, and NF-kappaB inhibitor beta. Over 100 proteins were identified by at least two peptides using a Mascot ion cut-off score of 30.

2018-10-19 | PXD001932 | Pride

The Aryl hydrocarbon receptor and FOS mediated cytotoxicity induced by Acenatobacter baumannii

Project description:Acinetobacter baumannii is a highly pathogenic and multidrug-resistant Gram-negative bacterium that causes severe nosocomial infections. To better understand the mechanism of pathogenesis, we compare the proteomes of uninfected and infected human cells, revealing that transcription factor FOS is the host protein most strongly induced by A. baumannii infection. Pharmacological inhibition of FOS reduces the cytotoxicity of A. baumannii in cell-based models, and similar results are also observed in a mouse infection model. A. baumannii outer membrane vesicles (OMVs) are shown to activate the aryl hydrocarbon receptor (AHR) of host cells by inducing the host enzyme tryptophan-2,3-dioxygenase (TDO), producing the ligand kynurenine, which binds AHR. Following ligand binding, AHR is a direct transcriptional activator of the FOS gene. Our results suggest that bacterial infection interacts with host tryptophan metabolism and the transcription factor FOS.

2024-08-05 | PXD053768 | Pride

RNA Sequencing looking at differential gene expression between p65+/+ and p65-/- mouse embryonic fibroblasts (MEFs)

Project description:We look at differential gene expression between immortalized p65+/+ and p65-/- MEFs to identify potential NF-kB regulated genes which when grouped based on biological function indicates candidates involved in protecting p65+/+ cells from macrophage-mediated killing

2017-10-01 | GSE101092 | GEO

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