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Gene expression on in vitro activated DCs

ABSTRACT: We have analyzed the effects of IL-27 signaling in dendritic cells (DCs) in the activation and polarization of effector and regulatory T cells, and the development of experimental autoimmune encephalomyelitis, an experimental model of multiple sclerosis. In this dataset, we include the results of treating DCs with IL-27.

ORGANISM(S): Mus musculus

PROVIDER: GSE49328 | GEO | 2013/07/30

SECONDARY ACCESSION(S): PRJNA213636

REPOSITORIES: GEO

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Gene expression on in vitro activated DCs

Project description:We have analyzed the effects of IL-27 signaling in dendritic cells (DCs) in the activation and polarization of effector and regulatory T cells, and the development of experimental autoimmune encephalomyelitis, an experimental model of multiple sclerosis. In this dataset, we include the results of treating DCs with IL-27. Primary splenic C57BL/6 DCs were isolated, cultured in vitro +/- IL-27 and RNA was prepared.

2013-07-30 | E-GEOD-49328 | biostudies-arrayexpress

Title: An IL-23-STAT4 Axis Regulates Classical Dendritic Cell Expansion and Function in Experimental Autoimmune Encephalomyelitis

Project description:The signal transducer and activator of transcription 4 (STAT4) promotes protective immunity and autoimmunity downstream of pro-inflammatory cytokines including IL-12 and IL-23. In experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), Stat4-/- mice are resistant to the development of inflammation and paralysis. Here, we examined cell-type requirements and found that in addition to T cells, STAT4 is required in dendritic cells for development of EAE. Deficiency of STAT4 in CD11c-expressing cells resulted in decreased T cell priming and inflammation in the CNS. EAE susceptibility was recovered following adoptive transfer of wild type bone marrow-derived DC to mice with STAT4-deficient DCs, but not adoptive transfer of STAT4- or IL-23R-deficient DCs. Single cell RNA-seq identified STAT4-dependent genes in DC subsets that paralleled a signature in MS patient DCs. Together, these data define a novel IL-23/DC/STAT4 pathway in DCs that could be a key to novel therapeutic targets in MS.

2024-07-17 | GSE243202 | GEO

Microarray expression data from monocytes, Mo-DCs and CD24 DCs

Project description:Cross-presentation of cell-associated antigens is carried out by classical DCs (cDCs) and monocyte-derived DCs (Mo-DCs), but whether a similar or distinct program exists for this process is unknown. In examining this issue, we discovered that only Ly-6ChiTremL4– monocytes, but not Ly-6ChiTremL4+ monocytes, can differentiate into Zbtb46+ Mo-DCs in response to GM-CSF and IL-4. However, Ly-6ChiTremL4+ monocytes were committed to Nur77-dependent development of Ly-6CloTremL4+ monocytes. Further, differentiation of monocytes with GM-CSF required addition of IL-4 to generate Zbtb46+ Mo-DCs that cross-presented as efficiently as CD24+ cDCs, which was accompanied by increased Batf3 and Irf4 expression. Unlike cDCs, Mo-DCs required only IRF4, and not Batf3, for cross-presentation. Further, Irf4–/– monocytes failed to develop into Zbtb46+ Mo-DCs, and instead developed into macrophages. Thus, cDCs and Mo-DCs use distinct transcriptional programs for cross-presentation that may drive different antigen-processing pathways. These differences may influence development of therapeutic DC vaccines based on Mo-DCs.

2016-05-25 | GSE75012 | GEO

Comparision of transcriptomes between murine WT type 1 conventional DCs to XCR1-deficient type 1 conventional DCs

Project description:We sought to compare the overall transcriptomic differences between TLR stimulated WT and XCR1-deficient type 1 conventional DCs. In addition, we also wanted to investigate functional role of XCR1 signaling in WT type 1 conventional DCs by treating recombinant murine XCL1, a ligand of XCR1 to these cells as well

2023-06-01 | GSE228392 | GEO

Cholera toxin mediates cAMP-dependent CTLA-2 secretion by dendritic cells to induce regulatory T cells in the EAE model

Project description:Therapy of autoimmune diseases by tolerogenic dendritic cells (DCs) represents an interesting option for clinical application. Mostly, immature or semi-mature stages of DCs have been shown to convert naïve T cells into FoxP3+ induced regulatory T cells (iTreg). Here we found that murine bone marrow-derived DCs (BM-DCs) matured with cholera toxin (CT) produced cytotoxic T lymphocyte antigen 2 (CTLA-2) via cAMP signaling. CTLA-2 is a cathepsin L inhibitor, however, it exerted cathepsin L-independent tolerogenic functions as shown with cathepsin L knock-out BM-DCs. High or low dose CT (CThi, CTlo) or cAMP treatment of BM-DCs, but not other stimuli such as LPS or TNF, induced mRNA of both isoforms of CTLA-2α and CTLA-2β. CThi-, CTlo- or cAMP-DCs display a mature phenotype (MHC IIhi, costimulationhi). Importantly, only CThi DCs secreted IL-1β, IL-6 and IL-23. Consequently, CThi DCs instructed Th17 cell polarization while, CTlo- or cAMP-DCs induced TGF-β-dependent FoxP3+ iTreg conversion but little or no Th17 cells. iTreg conversion could be reduced by blocking of CTLA-2 with siRNAs and in accordance, addition of recombinant CTLA-2α increased the conversion towards iTreg in vitro. Injection of CTlo- or cAMP-DCs exerted MOG peptide-specific protective effects in experimental autoimmune encephalomyelitis (EAE). Together, we identified CTlo- or cAMP-induced CTLA-2 production by BM-DCs as a tool to enhance their iTreg induction in vitro and in vivo. These findings point to CTLA-2 as a novel mediator of immune evasion by cholera bacteria and its potential use to treat autoimmune diseases.

2017-03-15 | GSE79274 | GEO

IL-33 stimulates DCs to express SEMA4A

Project description:IL-33 stimulates DCs to express SEMA4A

| PRJNA631212 | ENA

IFNγ signaling endows DCs with the capacity to control type I inflammation during parasitic infection through promoting T-bet+ regulatory T cells

Project description:Transcriptome analysis of IFNγ-insensitive DCs IFNγ signaling drives dendritic cells (DCs) to promote type I T cell (Th1) immunity. Here, we show that activation of DCs by IFNγ is equally crucial for the differentiation of a population of T-bet+ regulatory T (Treg) cells specialized to inhibit Th1 immune responses. Conditional deletion of IFNγ receptor in DCs but not in Treg cells resulted in a severe defect in this specific Treg cell subset, leading to exacerbated immune pathology during parasitic infections. Mechanistically, IFNγ-unresponsive DCs failed to produce sufficient amount of IL-27, a cytokine required for optimal T-bet induction in Treg cells. Thus, IFNγ signalling endows DCs with the ability to efficiently control a specific type of T cell immunity through promoting a corresponding Treg cell population.

2015-01-01 | GSE64594 | GEO

Interleukin-27 is a potent inhibitor of cis HIV-1 replication in Monocyte-derived Dendritic Cells via a Type I Interferon-independent pathway

Project description:IL-27 treated DCs were shown to be highly potent inhibitors of cis HIV-1, particularly of CCR5 tropic strains. Microarray studies of IL-27 treated DCs showed no up-regulation of Type I (IFN) gene expression. Neutralization of the Type-I IFN receptor had no impact on the HIV inhibition. Lastly, IL-27 mediated inhibition was shown to act post-viral entry and prior to completion of reverse transcription. These results show for the first time that IL-27 is a potent inhibitor of cis HIV-1 infection in DCs by a Type I IFN independent mechanism.

2013-03-29 | GSE44732 | GEO

Interleukin-27 is a potent inhibitor of cis HIV-1 replication in Monocyte-derived Dendritic Cells via a Type I Interferon-independent pathway

2013-03-29 | E-GEOD-44732 | biostudies-arrayexpress

Transcription profiling of mouse MBP Ac 11-11 activated purified CD4+ T cells

Project description:Local catabolism of the amino acid tryptophan (Trp) by indoleamine-2,3-dioxygenase (IDO) is considered an important mechanism of regulating T cell immunity. We show that IDO transcription was increased upon stimulation of myelin-specific T cells with tolerogenic altered self-peptides. Catabolites of Trp suppressed proliferation of myelin-specific T cells and inhibited production of proinflammatory TH1 cytokines. N-(3,4,-dimethoxycinnamoyl) anthranilic acid (3,4-DAA), an orally active synthetic derivative of the Trp metabolite anthranilic acid, reversed paralysis in mice with experimental autoimmune encephalomyelitis, a model of multiple sclerosis (MS). Trp catabolites and their derivatives offer a new strategy for treating TH1-mediated autoimmune diseases, such as MS. 4Y vd 1-11 comparison files are available as supplementary files. Experiment Overall Design: Double stranded cDNA was generated from total RNA extracted from MBP Ac 11-11 activated purified CD4+ T cells. Biotinylated cRNA was manufactured by in vitro transcription and hybridized to the Affymetrix genechip murine Mu11k set according to the manufacturer's protocols. Results were calculated as the ratio of mean average differences for each gene in 4Y versus Ac1-11 stimulated samples.

2008-06-12 | E-GEOD-3401 | biostudies-arrayexpress

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