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

ORGANISM(S): Homo sapiens

PROVIDER: GSE128113 | GEO | 2019/05/28

REPOSITORIES: GEO

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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.

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STAT1, STAT2 and IRF9 transcription factor binding analysis in wild type 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 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.

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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)

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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

The Cdkn2a gene product ARF is a critical regulator of IFNb mediated Lyme arthritis

Project description:Lyme disease is caused by infection with Borrelia burgdorferi, with a spectrum of clinical disorders. Murine studies with B6 and C3H mice have demonstrated that genetic differences in the host response play an essential role in regulating the severity of Lyme arthritis. C3H mice generate a robust induction of type I IFN response in joint tissue at one week of infection which leads to severe Lyme arthritis at 4 weeks post-infection, while B6 mice develop mild disease without a type I IFN profile. We used a forward genetic approach and identified B. burgdorferi arthritis- associated locus 1 (Bbaa1) on Chr4, which includes type I IFN cluster. B6.C3-Bbaa1 congenic mice display more severe Lyme arthritis than B6 mice. The blocking of type I IFN receptor and the IFNb subtype in Bbaa1 mice suppressed arthritis back to B6 level, so we concluded the Bbaa1 locus intrinsically controls IFNb production, and the differential expression of IFNb controls the severity of Lyme arthritis. However, the IFNb genes of C3H and B6 mice are identical, prompting focus on other genetic factors within the Bbaa1 locus as regulators of IFNb. Reciprocal radiation chimeras between B6.C3-Bbaa1 and B6 mice revealed myeloid cells in the joint tissue as IFNb initiators. Advanced congenic lines were generated to reduce the genetic contribution from C3H Bbaa1 region. RNA-seq of bone marrow-derived macrophages (BMDMs) from B6 and advanced interval specific recombinant congenic lines, ISRCL3 and ISRCL4, revealed novel candidates that may regulate Ifnb. In this study, we identify the Cdkn2a gene encoded ARF as a critical regulator of IFNb mediated Lyme arthritis, and investigate mechanistic interactions that modulate IFNb expression in Lyme arthritis development.

2022-02-17 | GSE181071 | GEO

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