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Transcription profile analysis of wild type and Irf9-/- bone marrow derived macrophages in response to type I and type II interferons

ABSTRACT: Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Our results show how mRNA expression changes upon IFNb or IFNg treatment in wild typ and Irf9-/- bone marrow derived macrophages.

ORGANISM(S): Mus musculus

PROVIDER: GSE115434 | GEO | 2019/05/28

REPOSITORIES: GEO

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Transcription profile analysis of wild type and Irf9-/- human monocytic THP1 cells in response to type I interferons

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Transcription profile analysis of wild type and Irf9-/- mouse embryonic fibroblasts (MEF) in response to type I interferons

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STAT1, STAT2 and IRF9 transcription factor binding analysis in wild type and Irf9-/- bone marrow derived macrophages in response to type I and type II interferons

Project description:Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Mechanisms to meet this demand on the relevant molecular machinery include remodeling of chromatin but also changes in transcription factor interaction prior and during the IFN response. Our results show how transcription factors STAT1, STAT2 and IRF9 change binding patterns upon IFNb or IFNg treatment in wild type and Irf9-/- bone marrow derived macrophages.

2019-05-28 | GSE115433 | GEO

STAT1, STAT2 and IRF9 transcription factor binding analysis in wild type human monocytic THP1 cells in response to type I interferons

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Homeostatic and Interferon-induced gene expression represent different states of promoter-associated transcription factor ISGF3

Project description:Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Mechanisms to meet this demand on the relevant molecular machinery include remodeling of chromatin but also changes in transcription factor interaction prior and during the IFN response. Our results show how distinct transcription factor complexes, determine the responsiveness of Interferon stimulated genes to different IRF9-containing complexes. Raw 264.7 macrophages expressing a doxycycline-inducible, myc-tagged versions of each IRF9-BirA*, STAT2-BirA* and STAT1-BirA* fusion genes were used to study complex formation in vivo. Furthermore, we extended the BioID proximity labeling by coupling it to parallel reaction monitoring to determine the degree and quantity of association between IRF9 and STATs in resting and interferon-treated macrophages.

2019-07-03 | PXD013209 | Pride

Homeostatic and Interferon-induced gene expression represent different states of promoter-associated transcription factor ISGF3

Project description:Host defense by the innate immune system requires the establishment of antimicrobial states allowing cells to cope with microorganisms before the onset of the adaptive immune response. Interferons (IFN) are of vital importance in the establishment of cell-autonomous antimicrobial immunity. Speed is therefore an important attribute of the cellular response to IFN. With much of the antimicrobial response being installed de novo, this pertains foremost to gene expression, the rapid switch between resting-state and active-state transcription of host defense genes. Mechanisms to meet this demand on the relevant molecular machinery include remodeling of chromatin but also changes in transcription factor interaction prior and during the IFN response. Our results show how distinct transcription factor complexes, determine the responsiveness of Interferon stimulated genes to different IRF9-containing complexes. Raw 264.7 macrophages expressing a doxycycline-inducible, myc-tagged versions of each IRF9-BirA*, STAT2-BirA* and STAT1-BirA* fusion genes were used to study complex formation in vivo. Furthermore, we extended the BioID proximity labeling by coupling it to parallel reaction monitoring to determine the degree and quantity of association between IRF9 and STATs in resting and interferon-treated macrophages.

2019-07-15 | PXD013251 | panorama

Chromatin accessibility analysis of wild type bone marrow-derived macrophages in response to Anisomycin, type I interferons and the combination of them or with p38 MAPK inhibitor PH-797804 (ATAC-Seq IFNb)

Project description:The innate immune system acts as the first line of defense against invasion of microbial pathogens. Here, macrophages play a substantial role in recognition, phagocytosis and killing of pathogens and the regulation of the innate immune response. Here, interferons play a crucial role in augmenting the antimicrobial functions of macrophages and their ability to produce mediators of immunoregulation. Pathogen recognition activates many different signaling pathways that interact to produce an innate response commensurate with the microbial challenge. The co-occurrence of signaling by sensors of stress and IFN receptors is a hallmark of innate responses to many viral and bacterial pathogens. Our results show changes in chromatin accessibility upon Anisomycin, a drug that induces stress-activation of MAPK pathways, IFNb stimulation and the combination of both or with p38 inhibitor PH-797804, Anisomycin and IFNb.

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Transcription profile analysis of wild type bone marrow derived-macrophages in response to Anisomycin, type I and type II interferons and the combination of them

Project description:The innate immune system acts as the first line of defense against invasion of microbial pathogens. Here, macrophages play a substantial role in recognition, phagocytosis and killing of pathogens and the regulation of the innate immune response. Here, interferons play a crucial role in augmenting the antimicrobial functions of macrophages and their ability to produce mediators of immunoregulation. Pathogen recognition activates many different signaling pathways that interact to produce an innate response commensurate with the microbial challenge. The co-occurrence of signaling by sensors of stress and IFN receptors is a hallmark of innate responses to many viral and bacterial pathogens. Our results show how Anisomycin, a drug that induces stress-activation of MAPK pathways, regulates mRNA expression of interferon stimulated genes (ISG) upon IFNg and IFNb stimulation

2022-12-18 | GSE199128 | GEO

The specifcity of innate immune response is enforced by repression of interferon-response elements by NFkB p50

Project description:The specific binding of transcription factors to cognate sequence elements is thought to be critical for the generation of specific gene expression programs. The transcription factors nuclear factor kB (NF-kB) and the interferon (IFN) regulatory factors (IRFs) bind to the kB site and the interferon response element (IRE), respectively, of target genes, and they are activated in macrophages after exposure to pathogens. However, how these factors produce pathogen-specific inflammatory and immune responses remains poorly understood. Combining top-down and bottom-up systems biology approaches, we have identified the NF-kB p50 homodimer (p50:p50) as a regulator of IRF responses. First, unbiased genome-wide expression analysis revealed that p50 repressed a subset of IFN-inducible genes through a previously uncharacterized subclass of guanine-rich IRE (G-IRE) sequences, which was substantiated by biochemical and structural analyses. Second, mathematical modeling predicted that p50:p50 might enforce the stimulus-specificity of composite promoters. Indeed, the production of the antiviral regulator IFN-b was rendered stimulus-specific by the binding of p50:p50 to the G-IRE–containing IFNb enhancer to suppress cytotoxic IFN signaling. Specifically, a deficiency in p50 resulted in the inappropriate production of IFN-b in response to bacterial DNA sensed by Toll-like receptor 9. This role for NF-kB p50 in enforcing the specificity of the cellular response to pathogens by binding to a previously uncharacterized subset of IRE sequences alters our understanding of how the NF-kB and IRF signaling systems cooperate to regulate antimicrobial immunity. [BMDM]: Total RNA extracted from wt, p50-/- or ifnar-/- bone marrow derived macrophages (BMDMs) were subjected to stimulation with LPS, CpG or IFNb [MEF]: Total RNA extracted from wt or p50KO primary mouse embryonic fibroblasts were subjected to stimulation with LPS or IFNb

2011-03-01 | E-GEOD-27112 | biostudies-arrayexpress

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