Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Interferon epsilon as a novel anti-viral agent in the testis [mouse]

ABSTRACT: The testis is susceptible to viral infections, which can impair fertility. Spermatogenic cells were thought to lack anti-viral defences, including interferon (IFN) or IFN-stimulated gene (ISG) expression. Challenging this dogma, we discovered that interferon-epsilon (IFNɛ), a type-I IFN first identified in female reproductive epithelia, is constitutively expressed by spermatogenic cells and macrophages in mouse and human testes. Moreover, mice lacking IFNɛ are more susceptible to viral epididymo-orchitis. The mechanisms of IFNɛ-mediated anti-viral protection in the testis were examined in this study.

ORGANISM(S): Mus musculus

PROVIDER: GSE253517 | GEO | 2024/10/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Interferon epsilon as a novel anti-viral agent in the testis [human]

Project description:The testis is susceptible to viral infections, which can impair fertility. Spermatogenic cells were thought to lack anti-viral defences, including interferon (IFN) or IFN-stimulated gene (ISG) expression. Challenging this dogma, we discovered that interferon-epsilon (IFNɛ), a type-I IFN first identified in female reproductive epithelia, is constitutively expressed by spermatogenic cells and macrophages in mouse and human testes. Moreover, mice lacking IFNɛ are more susceptible to viral epididymo-orchitis. The mechanisms of IFNɛ-mediated anti-viral protection in the testis were examined in this study.

2024-10-18 | GSE252991 | GEO

Interferon epsilon as a novel anti-viral agent in the testis

Project description:Interferon epsilon as a novel anti-viral agent in the testis

| PRJNA1065943 | ENA

Lavigne2021 - Non-spatial model of viral infection dynamics and interferon response of well-mixed viral infection

Project description:This ordinary differential equation model is described in the following article: "Autocrine and paracrine interferon signalling as ‘ring vaccination’ and ‘contact tracing’ strategies to suppress virus infection in a host" G. Michael Lavigne, Hayley Russell, Barbara Sherry and Ruian Ke DOI: 10.1098/rspb.2020.3002 Comment: This model is based on the ordinary differential equations of the non-spatial model of well-mixed viral infection stated in the manuscript (Eq. 2.1 in the article). Abstract: The innate immune response, particularly the interferon response, represents a first line of defence against viral infections. The interferon molecules produced from infected cells act through autocrine and paracrine signalling to turn host cells into an antiviral state. Although the molecular mechanisms of IFN signalling have been well characterized, how the interferon response collectively contribute to the regulation of host cells to stop or suppress viral infection during early infection remain unclear. Here, we use mathematical models to delineate the roles of the autocrine and the paracrine signalling, and show that their impacts on viral spread are dependent on how infection proceeds. In particular, we found that when infection is well-mixed, the paracrine signalling is not as effective; by contrast, when infection spreads in a spatial manner, a likely scenario during initial infection in tissue, the paracrine signalling can impede the spread of infection by decreasing the number of susceptible cells close to the site of infection. Furthermore, we argue that the interferon response can be seen as a parallel to population-level epidemic prevention strategies such as ‘contact tracing’ or ‘ring vaccination’. Thus, our results here may have implications for the outbreak control at the population scale more broadly.

2024-09-02 | BIOMD0000001021 | BioModels

Interferon epsilon as a novel anti-viral agent in the testis [mouse]

Project description:Interferon epsilon as a novel anti-viral agent in the testis [mouse]

| PRJNA1065946 | ENA

Interferon epsilon as a novel anti-viral agent in the testis [human]

Project description:Interferon epsilon as a novel anti-viral agent in the testis [human]

| PRJNA1063600 | ENA

Constitutive expression and distinct properties of IFN-epsilon protect the female reproductive tract from Zika virus infection.

Project description:The female reproductive tract (FRT) is vulnerable to sexually transmitted infections and therefore a well-tuned immune surveillance system is crucial for maintaining a healthy FRT. However, our understanding of the factors that impact viral infection of the FRT and the host response are not well understood. In this work, we investigate the role of a hormonally regulated type I interferon, IFN epsilon, in control of Zika virus (ZIKV) infection of the FRT. We demonstrate that IFN epsilon has anti-ZIKV properties using a combination of IFN epsilon KO mice, blockade of endogenous IFN epsilon by neutralising Abs and rescue of IFN epsilon KO mice by recombinant IFN epsilon administered directly to the FRT.

2023-02-14 | GSE223635 | GEO

IKK-epsilon regulates the balance between the type I and type II interferon responses

Project description:Virus infection induces the production of type I and type II interferons (IFN-I and IFN-II), cytokines that mediate the antiviral response. IFN-I (IFN-a and -b) induces the assembly of ISGF3 (interferon-stimulated gene factor 3), a multimeric transcriptional activation complex comprised of STAT1, STAT2 and IRF9. IFN-II (IFN-g) induces the homodimerization of STAT1 to form the GAF (gamma-activated factor) complex. ISGF3 and GAF bind specifically to distinct regulatory DNA sequences located upstream of IFN-I and II inducible genes, respectively, and activate the expression of distinct set of antiviral genes. The balance between the type I and type II IFN pathways plays a critical role in orchestrating the innate and adaptive immune systems. Here, we show that the phosphorylation of STAT1 by IKKε (IkB-related kinase epsilon) inhibits STAT1 homodimerization, and thus GAF formation, but does not disrupt ISGF3 formation. Therefore, virus and/or IFN-I activation of IKKε suppresses GAF-dependent transcription and promotes ISGF3-dependent transcription. In the absence of IKKε, GAF-dependent transcription is enhanced at the expense of ISGF3-mediated transcription, rendering cells less resistant to infection. We conclude that IKKε plays a critical role in regulating the balance between the IFN-I and IFN-II signaling pathways. ChIP-seq libraries were constructed with an antibody targeting STAT1 from bone marrow macrophages treated with interferon

2011-12-01 | E-GEOD-33913 | biostudies-arrayexpress

Transcription profiling of human epidermal keratinocytes treated with IFN-gamma reveals IFN-gamma suppressed the expression of over 100 genes responsible for cell cycle, DNA replication and RNA metabolism.

Project description:Cultured epidermal keratinocyte controls used for IFNg, TNFa and IL1 treatment. Interferon (IFN)-gamma, is a multifunctional, immunomodulatory cytokine with cell type-specific antiviral activities, particularly important in skin, where it is implicated in many diseases ranging from warts to psoriasis and cancer. Since epidermis is our first line of defence against many viruses, we investigated the molecular processes regulated by IFN-gamma in keratinocytes using DNA microarrays. We identified the IFN-gamma-regulated keratinocyte-specific genes in keratinocytes, IFN-gamma-induced tight junction proteins, presumably to deny viruses paracellular routes of infection. Furthermore, differing from published data, we find that IFN-gamma suppressed the expression of keratinocytes differentiation markers including desmosomal proteins, cornified envelope components and suprabasal cytokeratins. Inhibition of differentiation may interfere with the epidermal tropism of viruses that require differentiating cells for growth, for example, papillomaviruses. As in other cell types, IFN-gamma induced HLA, cell adhesion and proteasome proteins, facilitating leukocyte attraction and antigen-presentation by keratinocytes. IFN-gamma also induced chemokine/cytokines specific for mononuclear cells. IFN-gamma suppressed the expression of over 100 genes responsible for cell cycle, DNA replication and RNA metabolism, thereby shutting down many nuclear processes and denying viruses a healthy cell in which to replicate. Thus, uniquely in keratinocytes, IFN-gamma initiates a well-organized molecular programme boosting host antiviral defences, obstructing viral entry, suppressing cell proliferation and impeding differentiation.

2007-10-26 | E-GEOD-440 | biostudies-arrayexpress

Type-I interferon signatures in SARS-CoV-2 infected Huh7 cells

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes Coronavirus disease 2019 (COVID-19) has caused a global health emergency. A key feature of COVID-19 is dysregulated Interferon-response. Type-I interferon (IFN-I) is one of the earliest antiviral innate immune responses following viral infection and plays a significant role in pathogenesis of SARS-CoV-2. In this study, using a proteomics-based approach, we identified that SARS-CoV-2 infection induces delayed and dysregulated IFN-I signaling in Huh7 cells. We demonstrate that SARS-CoV-2 is able to inhibit RIG-I mediated IFN- production. Our results also confirm the recent findings that IFN-I pretreatment is able to reduce susceptibility of Huh7 cells to SARS-CoV-2, but not post-treatment. Senescent Huh7 cells in spite of showing accentuated IFN-I response were more susceptible to SARS-CoV-2 infection and SARS-CoV-2 effectively inhibited IFIT1 in these cells. Proteomic comparison between SARS-CoV-2, SARS-CoV and MERS-CoV revealed a distinct differential regulatory signature of interferon-related proteins emphasizing that therapeutic strategies based on observations in SARS-CoV and MERS-CoV should be used with caution. Our findings provide a better understanding of SARS-CoV-2 regulation of cellular interferon response and a perspective on its use as a treatment. Characterization of the role of different interferon stimulated genes on the inhibition of SARS-CoV-2 pathogenesis may direct novel antiviral strategies.

2021-05-18 | PXD023450 | Pride

Transcriptomic landscape of murine coronavirus infection in the lung

Project description:Impaired type I interferon (IFN) responses are predictive of severe disease during pulmonary coronavirus infection. Insufficient IFN-responsiveness is associated with viremia and hypercytokinemia, however the resolution of IFN-dependent innate immune responses in the lungs remains limited. Here, we aimed to elucidate the early dynamics of antiviral immunity and define the IFN-dependent mechanisms limiting viral spread during pulmonary infection with the murine coronavirus A59 (M-CoV-A59), a beta-coronavirus. Combining high-resolution transcriptomic analysis and genetic attenuation of interferon signaling, we delineated IFN-dependent cell-intrinsic and population-based transcriptional changes that determined viral replication and inflammatory maturation, respectively.

2023-01-02 | E-MTAB-11781 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data