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Gene expression of Dcir-/- dendritic cells (DCs) after antigen stimuulation

ABSTRACT: Purpose: DCIR is an inhibitory type of C-type lectin receptor that regulates DC functions. This study aimed to find the genes that could be regulated through DCIR. Method: Splenic DCs from WT and Dcir-/- mice were colutured with T cells that express specific TCR for MOG35-55 for 3 days in the presence of MOG peptide. CD11c+ cells were collected by an auto MACS. RNA profiles were generated by deep sequencing, in triplicate, using DNBSEQ-G400. Results: We detected xxx gense that were higher expression in Dcir-/- DCs, compared with WT DCs, with a fold change ≥1.5 and p value <0.05. Conclusion: Our data showed that Dcir deficiency in DCs changed the gene expression pattern, compared to WT DCs, in the coculture system of T cells. DCIR regulates the expression of DC genes that are associated with the functions of DCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE184068 | GEO | 2021/09/16

REPOSITORIES: GEO

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Gene expression of Dcir-/- osteoclasts induced by M-CSF and RANKL

Project description:Purpose: DCIR is an inhibitory type of C-type lectin receptor that regulates osteoclast (OC) formation and functions. This study aimed to find the genes of OCs that could be regulated through DCIR. Method: Bone marrow cells from WT and Dcir-/- mice were cultured in M-CSF for 2 days and the the cells were further cultured in M-CSF and RANKL. RNA profiles were generated by deep sequencing, in triplicate, using Illumina NovaSeq. Results: We detected xxx gense that were higher expression in Dcir-/- OCs, compared with WT OCs, with a fold change ≥1.5 and p value <0.05. Conclusion: Our data showed that Dcir deficiency in OCs changed the gene expression pattern, compared to WT OCs, which are induced by M-CSF and RANKL.

2023-06-07 | GSE223429 | GEO

Gene expression of murine iDCs isolated from tolerized MOG35-55-infused/MOG35-55-immunized or MOG35-55-immunized mice

2015-04-20 | GSE47210 | GEO

Gene expression of murine iDCs isolated from tolerized MOG35-55-infused/MOG35-55-immunized or MOG35-55-immunized mice

Project description:Recent data from our group, demonstrate that infusion of myelin oligodendrocyte glycoprotein (MOG35-55) peptide, leads to induction of MOG35-55-specific Tregs and subsequent suppression of Experimental Autoimmune Encephalomyelitis (EAE), the mouse model of multiple sclerosis. Amelioration of EAE was accompanied by reduced MOG-specific Th1 and Th17 responses in the draining lymph nodes (dLNs). Phenotypic analysis of the dLNs of MOG-infused mice revealed a significant Treg-mediated reduction in the recruitment of 7AAD-CD3-CD19-CD11c+CD11bhighGr-1+ iDCs compared to non-infused control immunized mice. Focusing on the delineation of novel molecules/genes that are involved in the MOG-specific Treg-mediated suppression of autoimmune responses, we have isolated highly purified iDCs from MOG infused and non-infused control immunized mice. Gene expression profiles of iDCs isolated from tolerized or immunized mice. Affymetrix MG 430 2.0 whole genome arrays were performed in triplicates for tolerized iDCs and immunized iDCs (6 arrays in total, 5 of them were analyzed). To obtain genes significantly regulated in iDCs upon tolerization with MOG35-55, the expression profiles of iDCs isolated from tolerized or immunized mice were compared to each other. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 µg cRNA hybridized to the 6 GeneChip arrays: Group1 iDCs isolated from tolerized mice, Group2 iDCs isolated from immunized mice.

2015-04-20 | E-GEOD-47210 | biostudies-arrayexpress

ATAC-seq data in MEF and mESC sequenced by BGI DNBSEQ-G400 platform and Illumina HiseqX10 instruments

Project description:We benchmark Illumina’s HiseqX10 instrument against Beijing Genomics Institute’s (BGI) DNBSEQ-G400 platform, a considerably cheaper sequencing alternative. For comparisons, the same bulk ATAC-seq libraries generated from pluripotent stem cells (PSCs) and fibroblasts were sequenced on both platforms. Both instruments generate sequencing reads with comparable mapping rates and genomic context. However DNBSEQ-G400 data contained a significantly higher number of small, sub-nucleosomal reads (>30% increase) and a reduced number of bi-nucleosomal reads (>75% decrease), which resulted in narrower peak-bases and improved peak calling, enabling the identification of 4% more differentially accessible regions between PSCs and fibroblasts. Ability to identify master TFs that underpin the PSC state relative to fibroblasts, including aggregate and de novo foot-printing capacity, were highly similar between data generated on both platforms.

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RNA-seq data in MEF and mESC sequenced by HiSeq 3000

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Expression data in splenic DC subsets in wild type and Xbp1 deficient mice

Project description:Xbp1 is a major transcription factor in the unfolded protein response. To uncover its function in DCs we generated a conditional KO for Xbp1 in dendritic cells. We here compare the expression of mRNAs in two different splenic DC subpopulations, CD8a and CD11b DCs in both WT and KO mice. Reference: Inositol-requiring enzyme 1-alpha regulates CD8a dendritic cell function via regulated mRNA decay. Osorio et al, Nature Immunology (2014) Primary DC subsets were isolated and sorted from spleens from 3 different WT or CD11c-cre Xbp-1fl/fl mice. RNA was isolated, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 1.0 ST Arrays (GPL6246).

2014-01-01 | E-GEOD-52857 | biostudies-arrayexpress

Expression data in splenic DC subsets in wild type and Xbp1 deficient mice

2014-01-01 | GSE52857 | GEO

Project description:Example data for interrupted runs on MGISEQ-2000 (now DNBSEQ-G400)

| PRJNA682569 | 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. We analyzed saliva from 3 WT DC samples and 3 IFNγR2 KO DC samples isolated from unmanipulated mice. In addition, we analyzed saliva from 3 WT DC samples and 3 IFNγR2 KO DC samples isolated from mixed BM chimeras (WT + IFNgR2KO) day 8 T. gondii infected.

2015-01-01 | E-GEOD-64594 | biostudies-arrayexpress

Transcriptional profile of WT, PRR and IFN-/- dendritic cells stimulated with poly IC in vivo

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.

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