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Transcriptome Profile of IEC4.1 cells deficient with Prdm1 in response to IFN-gamma

ABSTRACT: Transcriptome Profile of IEC4.1 cells deficient with Prdm1 in response to IFN-gamma

PROVIDER: PRJNA1027862 | ENA |

REPOSITORIES: ENA

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Transcriptome Profile of IEC4.1 cells deficient with Prdm1 in response to IFN-gamma

Project description:This study is to investigate the potential role of Prdm1 in murine intestinal epithelial cells (IEC4.1 cells) in response to IFN gamma stimulation. Prdm1 was knocked down in IEC4.1 cells by using a CRISPR/Cas9 approach. Wild type IEC4.1 cells were used as control (Ctrl). Cells were treated with or without mouse IFN gamma (1ng/ml for 4hrs). Then total RNA was collected for sequencing via DNBSEQ platform to obtain a comprehensive view of the transcriptome.

2025-05-30 | GSE245345 | GEO

Transcriptomic profile of IEC4.1 cells treated with an ASO to lncRNA XR_001779380 in response to IFN-gamma

Project description:LncRNAs may play an important role in intestinal epithelial cell autonomous defense against microbial infection. Our previous study showed that lncRNA XR_001779380 can interact with Prdm1 to modulate gene transcriuption in intestinal epithelial cells and may regualte IFN-gamma-stimulated gene transcription. Here we designed an antisense oligos-morpholine (ASO4) targeting the sequence of lncRNA XR_001779380 to interfere with its interaction with PRDM1. Murine intestinal epithelial cells (IEC4.1 cells) were treated with ASO4 or a standard control ASO-morpholine (ST) for 24h, followed by exposure to IFN-gamma (1 ng/ml) for 4 hours. Then total RNA was collected for sequencing via DNBSEQ platform to obtain a comprehensive view of the transcriptome.

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Transcriptomic profile of IEC4.1 cells treated with an siRNA to lncRNA NR_126553 (Nostril) in response to IFN-gamma protein (IFNγ)

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Analysis of WT and IRF1-deficient Th9 cell transcriptomes in the presence of IFN-gamma

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Transcriptomic profile of IEC4.1 cells treated with an ASO to lncRNA XR_001779380 in response to IFN-gamma

Project description:Transcriptomic profile of IEC4.1 cells treated with an ASO to lncRNA XR_001779380 in response to IFN-gamma

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human ESC-MSCs: IFN-γ-nontreated, IFN-γ-treated for 1 day, IFN-γ-treated for 3 days

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Interferon (IFN)-γ promotes monocyte-mediated lung injury during influenza pathogenesis

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Human IRF1 governs macrophagic IFN-γ immunity to mycobacteria

Project description:Inborn errors of human IFN-γ-dependent macrophagic immunity underlie mycobacterial diseases, whereas inborn errors of IFN-α/β-dependent intrinsic immunity underlie viral diseases. Both types of IFNs induce the transcription factor IRF1. We describe unrelated children with inherited complete IRF1 deficiency and early-onset, multiple, life-threatening diseases caused by weakly virulent mycobacteria and related intramacrophagic pathogens. 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-α/β immunity. In leukocytes or fibroblasts stimulated in vitro, IRF1-dependent responses to IFN-γ are, both quantitatively and qualitatively, much stronger than those to IFN-α/β. Moreover, IRF1-deficient mononuclear phagocytes do not control mycobacteria and related pathogens normally when stimulated with IFN-γ. By contrast, IFN-α/β-dependent intrinsic immunity to nine viruses, including SARS-CoV-2, is almost normal in IRF1-deficient fibroblasts. Human IRF1 is essential for IFN-γ-dependent macrophagic immunity to mycobacteria, but largely redundant for IFN-α/β-dependent antiviral immunity.

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