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Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (ChIP-Seq)

ABSTRACT: We predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway.

ORGANISM(S): Mus musculus

PROVIDER: GSE36241 | GEO | 2012/09/19

SECONDARY ACCESSION(S): PRJNA153161

REPOSITORIES: GEO

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Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (ChIP-Seq)

Project description:We predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway. C57BL/6 mice were obtained from Jackson Laboratories. Foxo3-/- mice in the FVB background were obtained from MMRRC and were backcrossed to C57BL/6 mice at least 5 times to generate congenic mice. C57BL/6 Foxo3+/- heterozygotes were intercrossed to generate Foxo3-/- mice. Mice were maintained at the animal facility of the Institute for Systems Biology and used at 8–12 weeks of age. All animals were housed and handled according to the approved protocols of University of Washington and Institute for Systems Biology's Institutional Animal Care and Use Committees.

2012-09-19 | E-GEOD-36241 | biostudies-arrayexpress

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses

Project description:This SuperSeries is composed of the following subset Series: GSE36241: Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (ChIP-Seq) GSE37051: Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (expression) Refer to individual Series

2012-09-19 | E-GEOD-37052 | biostudies-arrayexpress

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (expression)

Project description:We have used an unbiased systems approach to predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. We detected significantly increased transcription of a subset of interferon-stimulated genes (ISGs) under basal conditions in Foxo3-null macrophages when compared to their wild type (WT) counterparts, suggesting that FOXO3 functions as a repressor of these genes. Stimulation of Foxo3-null macrophages with poly-IC (PIC) further increased the levels of this subset of ISGs, and also revealed the transcription of additional ISGs. C57BL/6 mice were obtained from Jackson Laboratories. Foxo3-/- mice in the FVB background were obtained from MMRRC and were backcrossed to C57BL/6 mice at least 5 times to generate congenic mice. C57BL/6 Foxo3+/- heterozygotes were intercrossed to generate Foxo3-/- mice. Mice were maintained at the animal facility of the Institute for Systems Biology and used at 8-12 weeks of age. All animals were housed and handled according to the approved protocols of the University of Washington and Institute for Systems Biology's Institutional Animal Care and Use Committees. Bone marrow macrophages from wildtype and Foxo3 knock-out mice were stimulated with PIC or left untreated. 3 replicates per group.

2012-09-19 | E-GEOD-37051 | biostudies-arrayexpress

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses (expression)

2012-09-19 | GSE37051 | GEO

A FOXO3-IRF7 gene regulatory circuit limits inflammatory sequelae of antiviral responses.

Project description:Antiviral responses must be tightly regulated to defend rapidly against infection while minimizing inflammatory damage. Type 1 interferons (IFN-I) are crucial mediators of antiviral responses and their transcription is regulated by a variety of transcription factors; principal among these is the family of interferon regulatory factors (IRFs). The IRF gene regulatory networks are complex and contain multiple feedback loops. The tools of systems biology are well suited to elucidate the complex interactions that give rise to precise coordination of the interferon response. Here we have used an unbiased systems approach to predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription and we have further demonstrated that FOXO3, IRF7 and IFN-I form a coherent feed-forward regulatory circuit. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway that balances the beneficial effects and deleterious sequelae of the antiviral response.

| S-EPMC3556990 | biostudies-literature

Identification of a FOXO3/IRF7 circuit that limits inflammatory sequelae of antiviral responses

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-09-19 | GSE37052 | GEO

SREBP2 restricts osteoclast differentiation and activity by regulating IRF7 and limits inflammatory bone erosion.

Project description:Osteoclasts are multinucleated bone resorbing cells, and their dysregulation leads to pathological bone destruction. Osteoclast formation must be tightly regulated to prevent excessive bone loss and to minimize bone damage. SREBP2 is a key transcription factor for cholesterol biosynthesis and a sensor for intracellular lipids. However, how the crosstalk between SREBP2 and lipid metabolism contributes to osteoclasts has not been determined. Here, we reveal that SREBP2 is a negative regulator of osteoclastogenesis. Targeted deletion of SREBP2 in myeloid cells result in low bone mass and accelerates inflammatory bone destruction. SREBP2-mediated regulation of osteoclastogenesis is independent of its canonical function in cholesterol biosynthesis but is mediated, in part, by its downstream target, interferon regulatory factor (IRF)7. Taken together, our study highlights the SREBP2-IRF7 regulatory circuit forms as a negative feedback inhibitory loop in osteoclast differentiation that represents a novel mechanism to restrain deleterious pathological bone destruction.

2024-09-30 | GSE172007 | GEO

ChIP-seq for IRF7

Project description:We performed ChiP-Seq for IRF7 in GM-CSF induced bone-marrow cells. IRF7 ChIP-Seq in myeloid cells

2014-12-03 | E-GEOD-62697 | biostudies-arrayexpress

FOXO1 and FOXO3

Project description:FOXO1 and FOXO3

| PRJNA495066 | ENA

Transcriptional repression of IRF7 by MYC is critical for antiviral immune response in human pDC [GEN2.2]

Project description:Type I interferons (IFN) are crucial mediators of human innate and adaptive immunity and are massively produced from plasmacytoid dendritic cells (pDC). IRF7 is a critical regulator of type I IFN production when pathogens are detected by TLR7/9 in pDC. However, hyperactivation of pDC can cause life-threatening autoimmune diseases. To avoid the deleterious effects of aberrant pDC activation, tight regulation of IRF7 is required. Nonetheless, the detailed mechanisms of how IRF7 transcription is regulated in pDC are still elusive. To this end, we identified the global gene expression changes after stimulation of human primary pDC with the TLR9 agonist CpGB. We identified that the transcription factor MYC is prominently upregulated upon CpGB engagement in pDC. Moreover, when we knocked down MYC in the pDC-like cell line GEN2.2, production of interferon-stimulated genes (ISGs) was dramatically increased and was further enhanced by CpGB. Interestingly, MYC is shown to be recruited to the IRF7 promoter region through interaction with NCOR2/HDAC3 for its repression, and HDAC3 inhibition enhanced IRF7 expression and IFNβ production. Interestingly, activation of TLR9-mediated NF-kB and MAPK and nuclear translocation of IRF7 were greatly enhanced by MYC depletion. Pharmaceutical inhibition of MYC recovered IRF7 expression, further confirming the negative role of MYC in the antiviral response by pDC. Furthermore, the inverse correlation of MYC and IRF7 was validated in psoriasis skin sample datasets. Therefore, our results identify the novel immunomodulatory role of MYC in human pDC and may add to our understanding of aberrant pDC function in autoimmune diseases.

2016-11-30 | GSE70276 | GEO

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