Mus musculus
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ABSTRACT:
PROVIDER: PRJNA200593 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of the specific transcriptional changes on DCs provided by direct pattern recogition receptor (PRR) or IFNAR signaling that are required for DC maturation after poly IC stimulation. Results provide important information about the intricate differentiation process of DC maturation and the importance of type I IFNs for DC immunogenicity. WT/IFNA-/- or WT/PRR-/- mixed-chimera mice were injected with 50 ug Poly-IC i.p. in vivo 4 and 14 hr later, wild type and KO CD11chi CD3- DX5- B220- DCs were FACS sorted based on CD45.2 expression. Total RNA was isolated and expression profile was compared between unstimulated and activated WT and KO DCs.
2013-10-01 | E-GEOD-46478 | biostudies-arrayexpress
Project description:Analysis of the specific transcriptional changes on DCs provided by direct pattern recogition receptor (PRR) or IFNAR signaling that are required for DC maturation after poly IC stimulation. Results provide important information about the intricate differentiation process of DC maturation and the importance of type I IFNs for DC immunogenicity.
2013-10-01 | GSE46478 | GEO
Project description:The injection of the pathogen-associated molecular pattern Polyinosinic-polycytidylic acid (poly(I:C)) leads to the activation of various immune cells, including dendritic cells (DCs) and Natural Killer (NK) cells. This activation is due to different innate cytokines produced early after injection, in particular IFN-I. The objective of the study was to compare the pattern of expression of IFN-I stimulated genes between DC and NK cells. The project focused on a specific subset of conventional DC, CD8a DC, which responsiveness to IFN-I determines the capacity to activate CD8 T cells by cross-presentation of exogenous antigens. To identify the responses to IFN-I selectively induced in CD8a+ DC, we compared their gene expression profile to that of NK cells, using gene chips, before and after poly(I:C) stimulation. This study includes data from CD8a+ cDCs and NK cells purified by flow cytometry from the spleen of WT C57BL/6 mice, under steady-state conditions or 3 hours after administration of 100 ug poly(I:C) by intravenous injection. Two independent replicates were made for each cell type.
2012-10-17 | E-GEOD-39556 | biostudies-arrayexpress
Project description:Objective: Patients with Systemic Lupus Erythematosus (SLE) have an ongoing interferon (IFN) production due to an activation of plasmacytoid dendritic cells (pDCs), which can be triggered to type I IFN synthesis by RNA containing immune complexes (RNA-IC). Considering emerging data suggesting a role of type III interferon (IFN) in the SLE disease process, we asked if RNA-IC can induce type III IFN production in pDC, and how this production can be regulated. Methods: Peripheral blood mononuclear cells (PBMCs) or immune cell subsets were isolated from healthy blood donors or SLE patients and stimulated with IC containing U1 snRNP and SLE-IgG (RNA-IC). Hydroxychloroquine (HCQ) and an interleukin receptor 1 associated kinase 4 inhibitor (IRAK4i) were added to cell cultures. Cytokine mRNA levels were determined with a microarray and protein levels with immunoassays. Single-cell RNA-sequencing of pDCs using ddSEQ technology was performed. Results: Type III IFN mRNA and protein was induced in RNA-IC stimulated pDC-NK and pDC-B cell co-cultures. A subset of activated pDCs (3%) expressed both type III and type I IFN mRNA. IFN-λ2, IFN-α2b, interleukin (IL)-3, IL-6 or granulocyte-macrophage colony stimulating factor (GM-CSF) enhanced IFN-λ1/3 production 2-5-fold. HCQ and an IRAK4i blocked the RNA-IC-triggered IFN-λ1/3 production (p<0.01). IFN-α2b and GM-CSF increased the proportion of SLE patients producing IFN-λ1/3 in response to RNA-IC from 11 to 33%. Conclusions: Type III IFN production is triggered by RNA-IC in pDCs in a TLR-MyD88-dependent manner, enhanced by NK and B cells as well as several pro-inflammatory cytokines. These results support a contributing role for both type I and type III IFNs in SLE, which needs to be considered when targeting the IFN system in this disease.
2020-05-23 | GSE149415 | GEO
Project description:Objective: Patients with Systemic Lupus Erythematosus (SLE) have an ongoing interferon (IFN) production due to an activation of plasmacytoid dendritic cells (pDCs), which can be triggered to type I IFN synthesis by RNA containing immune complexes (RNA-IC). Considering emerging data suggesting a role of type III interferon (IFN) in the SLE disease process, we asked if RNA-IC can induce type III IFN production in pDC, and how this production can be regulated. Methods: Peripheral blood mononuclear cells (PBMCs) or immune cell subsets were isolated from healthy blood donors or SLE patients and stimulated with IC containing U1 snRNP and SLE-IgG (RNA-IC). Hydroxychloroquine (HCQ) and an interleukin receptor 1 associated kinase 4 inhibitor (IRAK4i) were added to cell cultures. Cytokine mRNA levels were determined with a microarray and protein levels with immunoassays. Single-cell RNA-sequencing of pDCs using ddSEQ technology was performed. Results: Type III IFN mRNA and protein was induced in RNA-IC stimulated pDC-NK and pDC-B cell co-cultures. A subset of activated pDCs (3%) expressed both type III and type I IFN mRNA. IFN-λ2, IFN-α2b, interleukin (IL)-3, IL-6 or granulocyte-macrophage colony stimulating factor (GM-CSF) enhanced IFN-λ1/3 production 2-5-fold. HCQ and an IRAK4i blocked the RNA-IC-triggered IFN-λ1/3 production (p<0.01). IFN-α2b and GM-CSF increased the proportion of SLE patients producing IFN-λ1/3 in response to RNA-IC from 11 to 33%. Conclusions: Type III IFN production is triggered by RNA-IC in pDCs in a TLR-MyD88-dependent manner, enhanced by NK and B cells as well as several pro-inflammatory cytokines. These results support a contributing role for both type I and type III IFNs in SLE, which needs to be considered when targeting the IFN system in this disease.
2020-05-23 | GSE148902 | GEO
Project description:RNAseq of control vs poly-IC treated A549 cells shows IFN induction.
2018-09-25 | GSE120355 | GEO
Project description:Analysis of changes in gene expression after incubation of dendritic cells with immune complexes or medium. Since the dendritic cells are derived from three different mouse strains, either wild type, Fcγ receptor IIb KO (expresses only activating Fcγ receptors) or Fc receptor γ chain KO (expresses only inhibitory Fcγ receptor), the analysis gives important insight into the roles of the activating versus inhibiting Fcγ receptors on dendritic cells. Bone marrow-derived dendritic cells of the three mouse genotypes (see above) were incubated for 4 hours with medium (unstimulated) or OVA-anti OVA immune complexes (IC, stimulated) and changes in gene expression after stimulation with IC were compared between unstimulated vs stimulated with IC and across the three genotypes.
2012-05-02 | E-GEOD-33718 | biostudies-arrayexpress
Project description:The injection of the pathogen-associated molecular pattern Polyinosinic-polycytidylic acid (poly(I:C)) leads to the activation of various immune cells, including dendritic cells (DCs) and Natural Killer (NK) cells. This activation is due to different innate cytokines produced early after injection, in particular IFN-I. The objective of the study was to compare the pattern of expression of IFN-I stimulated genes between DC and NK cells. The project focused on a specific subset of conventional DC, CD8a DC, which responsiveness to IFN-I determines the capacity to activate CD8 T cells by cross-presentation of exogenous antigens. To identify the responses to IFN-I selectively induced in CD8a+ DC, we compared their gene expression profile to that of NK cells, using gene chips, before and after poly(I:C) stimulation.
2012-10-17 | GSE39556 | GEO
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:The present study reveals LMYC and MXD1 as novel regulators of a transcriptional program that is modulated during the maturation of Batf3-dependent dendritic cells (also known as type I classical dendritic cells or cDC1s). We used microarray analysis with ERCC spike in controls to determine the transcriptional effects of MYCL and MXD1 deficiency at steady state and after activation with poly IC. Mycl-deficient mice are available from Jackson laboratories as B6.129S6(C)-Mycltm1.1Kmm/J. Mxd1-/- mice were provided by R. Eisenman.
2019-12-05 | GSE141492 | GEO