Expression data from the comparison between poly(I:C)-treated WT and Oasl1-/- BMDMs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE41788 | GEO | 2013/02/17
SECONDARY ACCESSION(S): PRJNA178177
REPOSITORIES: GEO
Similar Datasets
Project description:Oasl1-/- BMDMs express more type I IFN upon poly(I:C) treatment. Because OASL1 seems to rather specifically suppress the type I IFN expression, we tried to address the specificity by determining the defects associated with the Oasl1 mutation using genome-wide gene expression microarray analysis under moderate poly(I:C) stimulation (5 µg/ml for 9 h); this condition was used to identify the primary targets of OASL1 while minimizing the secondary targets induced by the earlier, higher production of type I IFNs in Oasl1-/- cells. Only 23 genes out of approximately 35,000 probed transcripts showed a signal difference greater than two-fold between the WT and KO cells; 15 showed higher signals in KO cells while 8 showed lower signals in KO cells We analyzed total RNA from poly(I:C)-treated WT and Oasl1-/- BMDM using the Affymetrix Mouse Gene 1.0 ST array. Array data were processed by Affymetrix GCOS software. We compared these using Affymetrix Expression console1.1, TMEV4.4, DAVID.
2013-02-17 | E-GEOD-41788 | biostudies-arrayexpress
Project description:OASL1 is a novel translation inhibitor for the type I IFN master transcription factor IRF7. To examine whether OASL1 specifically inhibit IRF7 translation, we used a genome-wide gene expression microarray to screen for the polysome-associated mRNAs more enriched in the OASL1 KO BMDMs. The microarray analysis on the polysomal fractions identified 145 candidate transcripts, including IRF7, that showed a signal greater than two-fold higher in poly(I:C)-treated Oasl1-/- BMDM.
2013-02-17 | GSE41787 | GEO
Project description:OASL1 is a novel translation inhibitor for the type I IFN master transcription factor IRF7. To examine whether OASL1 specifically inhibit IRF7 translation, we used a genome-wide gene expression microarray to screen for the polysome-associated mRNAs more enriched in the OASL1 KO BMDMs. The microarray analysis on the polysomal fractions identified 145 candidate transcripts, including IRF7, that showed a signal greater than two-fold higher in poly(I:C)-treated Oasl1-/- BMDM. We analyzed polysomal fractions from poly(I:C)-treated WT and Oasl1-/- BMDM using the Affymetrix Mouse Gene 1.0 ST array. Array data were processed by Affymetrix GCOS software. We compared these using Affymetrix Expression console1.1, R affy-package(2.9.2), DAVID.
2013-02-17 | E-GEOD-41787 | biostudies-arrayexpress
Project description:The Pim (proviral integration site for Moloney murine leukemia virus) proteins form a serine threonine kinase family that regulates cell proliferation, migration and cell survival. Here we demonstrate for the first time that a Pim1 kinase plays an essential role in antiviral innate immune responses. Specifically, our in vivo, in vitro and RNA-sequencing analyses showed that Pim1 was quickly upregulated after Toll-like receptor (TLR) stimulation in a NF-kB-dependent manner and then promoted IFN-b production by forming a cell-surface complex composed of TRIF-signaling molecules and IRF3 that promoted IRF3 phosphorylation, nuclear translocation, and IFN-b production. As shown by Pim1 knockdown and knockout, Pim1 was essential for this role but its kinase activity was not involved. Pim1-deficiency increased the susceptibility of mice to poly I:C-induced sepsis. Our study uncovers a previously unrecognized role for Pim1 in antiviral innate immune responses, thus providing a new target for controlling viral infection.
2022-12-14 | GSE195582 | GEO
Project description:To explore the influence of IFNR-mediated singnaling in ISCs, we performed microarray analysis of the ISCs from control Lgr5ki mice versus Ifnar1-/-Lgr5ki mice after treating for 1 weeks with low doses of poly(I:C), which potentially induce type I and -III IFNs. The Gene Ontology (GO) analysis indicated that the GO terms overrepresented among the genes upregulated in ISCs from poly(I:C)-treated WT mice compared with those from poly(I:C)-treated Ifnar1−/− mice included “defense response to virus”, “immune system process”, “response to virus”, and “innate immune response”, all from the GOTERM_Biological Processes (BP) category. We compared these results against the Interferome database, which contains genes regulated by type I, II, or III IFN, compiled by analyzing the expression data of IFN-treated cells (http://www.interferome.org), and found that most of the genes found for the GO term “defense response to virus” were IFN-inducible genes, indicating that IFNs act directly on ISCs. The GO analysis also showed an enrichment of defense response to bacteria. In the GOTERM_Cellular Component (CC) category, “extracellular space” and “extracellular region” ranked at the top, indicating a dramatic change in the expression pattern of secretory molecules. Notably, these GO terms included genes encoding antibacterial proteins and endocrine hormones such as angiogenin, defensin, lysozyme, chromogranin, and glucagon, all of which are produced by secretory IECs. Thus, we hypothesized that excess IFN signals force ISCs to lose stemness and differentiate into secretory progenitors.
2020-07-21 | GSE137189 | GEO
Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.
2018-11-07 | PXD011577 | Pride
Project description:Type I conventional dendritic cells (cDC1s) are an essential antigen-presenting population, required for generating adaptive immunity against intracellular pathogens and tumors. While the transcriptional control of cDC1 development is well understood, the mechanisms by which extracellular stimuli affect cDC1 function remain unclear. Recently, we demonstrated that the cytokine IL-10 inhibits cDC1 maturation induced upon polyinosinic-polycytidylic acid (poly I:C) exposure via a STAT3-dependent mechanism. Furthermore, utilizing a tumor vaccine strategy, we found STAT3 restrains cDC1-mediated anti-tumor immunity. To understand the pathways by which IL-10 and STAT3 regulate cDC1s, we evaluated transcriptional responses by RNA-sequencing. Bioinformatic analyses indicated that many inflammatory pathways were enriched in cDC1s following poly I:C treatment, while interferon (IFN) signaling was uniquely inhibited by STAT3 upon concomitant exposure to IL-10. We found that poly I:C stimulated production of IFN-b and IFN-g from cDC1s. Concurrent exposure to IL-10 suppressed IFN-b and IFN-g secretion as well as accrual of phosphorylated STAT1 and expression of the IFN-response gene Cxcl10 in cDC1s. By contrast, Stat3-deficient cDC1s were refractory to IL-10, indicating STAT3 controls poly I:C-mediated IFN production and IFN transcriptional responses in cDC1s. Moreover, we found that maturation of cDC1s in response to poly I:C is dependent on the type I IFN receptor. Taken together, our data indicate STAT3 is essential for restraining autocrine type I IFN signaling in cDC1s elicited by poly I:C stimulation.
2022-07-26 | GSE188995 | GEO
Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-α in vitro and that Siglec-H ko mice produce more IFN-α after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease. For microarray experiments gene expression profiles of total splenic cells from two wt and Siglec-H ko mice 26 weeks after infection with luciferase expressing murine Cytomegalovirus (5x105 pfu) or from two uninfected wt and Siglec-H ko control mice were analyzed
2016-03-16 | E-GEOD-79248 | biostudies-arrayexpress
Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-α in vitro and that Siglec-H ko mice produce more IFN-α after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease.
2016-03-16 | GSE79248 | GEO
Project description:We provide gene expression data of wild-type (WT) and various knock-out (KO) bone marrow derived macrophages (BMDMs) from mice (C57BL/6) in different conditions of infections and treatments. We included BMDMs from WT (female and male), Ifnar-/-, IFNg-/-, iNOs-/-, Nlrx1-/- (female and male), Nox2-/- and Prx5-/- mice. BMDMs were either infected with a human protozoan parasite Leishmania guyanensis with or without its endosymbiant double-stranded RNA (dsRNA) virus, Leishmania RNA Virus 1 (LgyLRV1+ and LgyLRV1-, respectively). Alternatively BMDMs were treated with a TLR3 agonist poly I:C, a TLR2 agonist FSL1, with H2O2 or tBHQ.
2022-04-20 | GSE201066 | GEO