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Virus Mimicry in the Tumor Microenvironment Activates RIG-I Through Unshielding of Endogenous RNA in Exosomes [ppp5end RNA-Seq]

ABSTRACT: The goal of this study is to investigate if endogenous RNA in exosomes activates RIG-I through unshielding.

ORGANISM(S): Homo sapiens

PROVIDER: GSE93073 | GEO | 2017/07/01

SECONDARY ACCESSION(S): PRJNA359793

REPOSITORIES: GEO

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Virus Mimicry in the Tumor Microenvironment Activates RIG-I Through Unshielding of Endogenous RNA in Exosomes [RNA-Seq]

Project description:The goal of this study is to investigate if endogenous RNA in exosomes activates RIG-I through unshielding.

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Virus Mimicry in the Tumor Microenvironment Activates RIG-I Through Unshielding of Endogenous RNA in Exosomes [exoRNA-Seq]

Project description:The goal of this study is to investigate if endogenous RNA in exosomes activates RIG-I through unshielding.

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Virus Mimicry in the Tumor Microenvironment Activates RIG-I Through Unshielding of Endogenous RNA in Exosomes

Project description:Virus Mimicry in the Tumor Microenvironment Activates RIG-I Through Unshielding of Endogenous RNA in Exosomes

| PRJNA359789 | ENA

Virus Mimicry in the Tumor Microenvironment Activates RIG-I Through Unshielding of Endogenous RNA in Exosomes

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

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RIP-Seq and RNA-Seq of an RNA-binding protein secreted by Listeria monocytogenes which activates RIG-I signaling

Project description:Secreted bacterial RNAs have recently emerged as a novel host-pathogen interaction mode. Naked RNA molecules are highly labile in the extracellular environment and must be protected by packaging into membrane vesicles or into complexes with RNA binding proteins. RNA secretion through membrane vesicles has been shown for several bacterial species but, surprisingly, proteins that bind and stabilize bacterial RNAs in the extracellular environment have not been reported yet. Here, we show that the bacterial pathogen L. monocytogenes secretes a small RNA binding protein that we named Zea. We show that Zea binds and stabilizes a subset of L. monocytogenes RNA, causing its accumulation in the extracellular medium. Zea modulates L. monocytogenes in vivo. Furthemore, Zea binds the mammalian non-self-RNA innate immunity sensor RIG-I and potentiates RIG-I-signaling during infection. This study provides a mechanism for the stability of extracellular RNA and unveils how secreted bacterial RNAs participate in the host-pathogen crosstalk.

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TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment II

Project description:Telomerase plays a pivotal role in tumorigenesis by both telomere-dependent and telomere-independent activities, although the underlying mechanisms are not completely understood. Using single-sample gene set enrichment analysis (ssGSEA) across 9,264 tumour samples, we observed that expression of telomerase reverse transcriptase (TERT) is closely associated with immune-suppressive signatures. We demonstrated that TERT can activate a subclass of endogenous retroviruses (ERVs) to form double-stranded RNAs (dsRNAs), which were sensed by the RIG-1/MDA5-MAVS signalling pathway and triggered interferon signalling in cancer cells. Furthermore, we showed that TERT-induced ERVs/interferon signalling stimulated the expression of chemokines, including CXCL10, which induced suppressed T cell infiltration with increased percentage of CD4+ and FOXP3+ cells. These data reveal an unanticipated role for telomerase as a transcriptional activator of ERVs and provide strong evidence that TERT-mediated ERVs/interferon signalling contributes to immune suppression in tumours.

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TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment I

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TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment III

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Identification of avian RIG-I responsive genes during influenza infection

Project description:Transcriptional profiling of chicken embryonic fibroblasts (DF-1 cells) comparing the effects of chicken cells transfected with duck RIG-I compared to empty-vector transfected cells following with low or highly pathogenic avian influenza. Goal was to determine the effects of duck RIG-I on influenza-induced immune gene expression. Two-condition experiment. Biological replicates for low pathogenic avian influenza infection: 3 empty-vector transfected replicates, 3 RIG-I transfected replicates. Biological replicates for highly pathogenic influenza infection: 2 empty-vector transfected replicates, 2 RIG-I transfected replicates.

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