MicroRNA changes during pDC activation
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE21160 | GEO | 2013/03/25
SECONDARY ACCESSION(S): PRJNA126611
REPOSITORIES: GEO
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Project description:To identify microRNA changes during plasmacytoid dendritic cell (PDC) activation, we stimulated human primary PDCs with 10ug/ml R837 (Invivogen, San Diego, CA, USA) for 4 hours. Purified human pDCs were divided into two parts: one was cultured with medium alone, another was cultured with R837. 4 hours later, cells were collected and total RNA was extracted for the TaqManM-BM-. Human MicroRNA Arrays. The experiment was duplicated (sample1 and sample2).
2013-03-25 | E-GEOD-21160 | biostudies-arrayexpress
Project description:Plasmacytoid dendritic cells (pDCs) were initially considered as critical for innate immunity to viruses. However, our group has shown that pDCs bind to and inhibit the growth of Aspergillus fumigatus hyphae and that depletion of pDCs renders mice hypersusceptible to experimental aspergillosis. In this study, we examined pDC receptors responsible for hyphal recognition and downstream events in pDCs stimulated by A. fumigatus hyphae. Our data show that Dectin-2 but not Dectin-1 participates in hyphal recognition by pDCs and that Dectin-2 acts in cooperation with the FcRγ chain to trigger signaling responses. In addition, using confocal and electron microscopy we demonstrated that the interaction between pDCs and A. fumigatus induced the formation of pDC extracellular traps (pETs) containing DNA and citrullinated histone H3. Thus, these structures closely resembled those of neutrophil extracellular traps (NETs). Microarray analysis of the pDC transcriptome upon A. fumigatus infection demonstrated up-regulated expression of genes previously associated with viral infections or apoptosis. Moreover, the abundant expression of type I Interferon-encoding genes seen in CpG-stimulated pDCs was absent in the pDCs infected with A. fumigatus hyphae. Thus, human pDCs directly recognize A. fumigatus hyphae via Dectin-2. This interaction leads to formation of pET and triggers a distinct pattern of pDC gene expression. The spectrum of changes in gene expression was examined in pDCs from 3 blood donors, 2 and 4h following incubation with hyphae. Comparative controls included unstimulated and CpG-stimulated pDCs.
2014-03-01 | E-GEOD-55467 | biostudies-arrayexpress
Project description:Committed precursors of conventional dendritic cells (pre-cDCs) derived from the common DC progenitor which differentiate into cDC subpopulations in peripheral tissues have been identified, but committed precursors for plasmacytoid DCs (pDCs) have not been found. Here we show that CDP-derived ‘CCR9- MHCIIlow BST2+ Siglec-H+ pDCs from murine bone marrow which enter the circulation and peripheral tissues have a common DC precursor function in vivo in the steady state. Upon adoptive transfer the fate of CCR9- pDC-like precursors is governed by the tissues they enter. In the bone marrow and liver most transferred CCR9- pDC-like precursors differentiate into CCR9+ pDCs, whereas in peripheral lymphoid organs, lung and intestine they can give rise to CCR9+ pDCs and cDCs. Thus, CCR9- pDC-like cells are novel CDP-derived circulating DC precursors with pDC and cDC potential, whose final differentiation depends on tissue-specific factors allowing adaptation to local requirements. Total RNA obtained from CCR9- pDC-like common DC progenitors and CCR9+ pDCs was compared for differential gene expression. 3 independent isolations were performed for the 2 samples. 6 arrays were run in total.
2012-05-15 | E-GEOD-37996 | biostudies-arrayexpress
Project description:Plasmacytoid dendritic cells (pDCs) were initially considered as critical for innate immunity to viruses. However, our group has shown that pDCs bind to and inhibit the growth of Aspergillus fumigatus hyphae and that depletion of pDCs renders mice hypersusceptible to experimental aspergillosis. In this study, we examined pDC receptors responsible for hyphal recognition and downstream events in pDCs stimulated by A. fumigatus hyphae. Our data show that Dectin-2 but not Dectin-1 participates in hyphal recognition by pDCs and that Dectin-2 acts in cooperation with the FcRγ chain to trigger signaling responses. In addition, using confocal and electron microscopy we demonstrated that the interaction between pDCs and A. fumigatus induced the formation of pDC extracellular traps (pETs) containing DNA and citrullinated histone H3. Thus, these structures closely resembled those of neutrophil extracellular traps (NETs). Microarray analysis of the pDC transcriptome upon A. fumigatus infection demonstrated up-regulated expression of genes previously associated with viral infections or apoptosis. Moreover, the abundant expression of type I Interferon-encoding genes seen in CpG-stimulated pDCs was absent in the pDCs infected with A. fumigatus hyphae. Thus, human pDCs directly recognize A. fumigatus hyphae via Dectin-2. This interaction leads to formation of pET and triggers a distinct pattern of pDC gene expression.
2014-03-01 | GSE55467 | GEO
Project description:Committed precursors of conventional dendritic cells (pre-cDCs) derived from the common DC progenitor which differentiate into cDC subpopulations in peripheral tissues have been identified, but committed precursors for plasmacytoid DCs (pDCs) have not been found. Here we show that CDP-derived ‘CCR9- MHCIIlow BST2+ Siglec-H+ pDCs from murine bone marrow which enter the circulation and peripheral tissues have a common DC precursor function in vivo in the steady state. Upon adoptive transfer the fate of CCR9- pDC-like precursors is governed by the tissues they enter. In the bone marrow and liver most transferred CCR9- pDC-like precursors differentiate into CCR9+ pDCs, whereas in peripheral lymphoid organs, lung and intestine they can give rise to CCR9+ pDCs and cDCs. Thus, CCR9- pDC-like cells are novel CDP-derived circulating DC precursors with pDC and cDC potential, whose final differentiation depends on tissue-specific factors allowing adaptation to local requirements.
2012-05-16 | GSE37996 | GEO
Project description:CpG 1826 binds to Toll-like receptor (TLR)9, whereas influenza virus PR8 activates pDC via TLR7. Differential stimulation of pDCs is expected to result in unique activation mechanism(s) leading to a different phenotypically and functionally matured pDC; We used microarrays to detail the global programme of gene expression underlying the maturation process of pDC activated with CpG 1826 and influenza virus PR8. We identified a distinct expression profile of upregulated immunomediators. Experiment Overall Design: Sorted pDCs were cultured for 1h and 4hs in medium control or with 5 µg/ml CpG 1826 or 300 HAU/ml purified influenza A/PR/8 virus. The first experiment (e1) included pDC in media and stimulated with CpG for 4h. In two other independent experimental batches (e2 and e3), we obtained samples of sorted pDC cultured in medium alone (med), and with CpG or PR8 (flu) for 1h and 4h. RNA extraction was performed using the RNeasy Kit (Qiagen) and hybridization on Affymetrix microarrays was performed using standard protocols. We sought to obtain homogeneous populations of pDCs at different time points under defined activation conditions in order to decipher the temporal resolution of expression profiles during the process of their maturation.
2008-06-15 | E-GEOD-7831 | biostudies-arrayexpress
Project description:Plasmacytoid dendritic cells (pDCs) have been shown to play an important role during immune responses, ranging from initial viral control through the production of type I interferons (IFNs) to antigen presentation. However, recent evidence uncovered unexpected heterogeneity among pDCs. Notably we identified a new subset, referred to as pDC-like cells, that resembles pDCs but shares cDC features. Here we show that this subset is a circulating progenitor distinct from common DC progenitors (CDP), with prominent cDC2 precursor potential. This precursor subset responds to homeostatic cytokines, such as macrophage colony stimulating factor (M-CSF) by expanding and differentiating into cDC2 that efficiently prime Th17 cell. Development of pDC-like cells into CX3CR1+ESAM- cDC2b but not CX3CR1- ESAM+ cDC2a requires the transcription factor KLF4. Finally, we show that under homeostatic conditions this developmental pathway regulates the immune threshold at barrier sites, by controlling the pool of Th17 cells within the skin draining lymph nodes.
2023-02-24 | GSE223100 | GEO
Project description:Autoantibodies to nuclear antigens are hallmarks for diagnosis of the autoimmune disease systemic lupus erythematosus (SLE) and they contribute to SLE pathogenesis. However, there remains a gap in our knowledge regarding how different isotypes of autoantibodies contribute to key disease processes, including the production of the critical type I interferon (IFN) cytokines by plasmacytoid dendritic cells (pDCs) in response to immune complexes (ICs). Here, we show that individuals with SLE have IgA autoantibodies against most nuclear antigens assessed, largely correlating with the amounts of IgG against the same antigen. We investigated whether IgA autoantibodies against a major SLE autoantigen, Smith ribonucleoproteins (Sm/RNPs), play a role in IC activation of pDCs. We found that pDCs express the IgA-specific Fc receptor, FcRI, and there was a striking ability of IgA1 isotype autoantibodies to synergize with IgG in RNA-containing ICs to generate robust pDC IFN responses. pDC responses to these ICs required both FcRI and FcRIIa, suggesting the most potent ICs for pDCs contained autoantibodies of both isotypes. Sm/RNP IC binding to and internalization by pDCs were greater when ICs contained both IgA1 and IgG. In addition, binding of Sm/RNP ICs generated with IgA1-sufficient serum correlated to pDC FcRI expression, but not FcRIIa expression. pDCs from individuals with SLE had higher binding of IgA1-containing ICs and higher expression of FcRI than pDCs from healthy control individuals, correlating with expression of IFN response genes. Taken together, our data indicate that IgA1 ANAs contribute to SLE pathology and warrant further investigation.
2023-10-19 | GSE242721 | GEO
Project description:Purpose: Taurine promotes the activation of plasmacytoid dendritic cells. The goals of this study are to identify genes and pathways invovled in the regulation. Methods: Mouse plasmacytoid dendritic cells were stimulated with R837, together with or without taurine for 12 hours. Then, the next-generation libraries of mRNA were prepared using VAHTS mRNA-seq v2 Library Prep Kit for Illumina® (Vazyme, Nanjing, China). The Library quality was determined by Bioanalyzer 4200 (Agilent, Santa Clara, CA, USA). Then the mRNA-seq libraries were sequenced in HiSeq ⅹ10 system (Illumina, San Diego, CA, USA) on a 150bp paired-end run. The differentially expressed genes were selected as having more than 1 fold difference in their geometrical mean expression between the compared groups and a statistically significant p-value (<0.05) by analysis of DEseq2. The GO analysis on differentially expressed genes was performed with an R package: Clusterprofiler using a p<0.05 to define statistically enriched GO categories. Pathway analysis was used to determine the significant pathway of the differential genes according to Kyoto Encyclopedia of Genes and Genomes Database (http://www.genome.jp/kegg/) and DAVID Bioinformatics Resources 6.8 (https://david.ncifcrf.gov/). Results: Genes in the TLR7-IRF7 pathway were augmented by taurine. As a result, the production of type I IFNs increased upon taurine treatment.
2020-02-20 | GSE145546 | GEO
Project description:Purpose: The goals of this study are to compare NGS-derived pDC transcriptome profiling (RNA-seq) normalized counts and differential expression of genes between different pDC states (steady state, or TLR9 activated for 2h, 6h, or 12h with CpG) in Batf presence and absence. Methods: mRNA profiles of Bone marrow-derived Flt3-L cultured FACS purified pDCs from wild-type and Batf-knockout mice that were left naive or stimulated with TLR9 agonist CpG for 2h, 6h r 12h were generated by deep sequencing, in triplicate, using the Illumina HiSeq3000 platform. DNase digested total RNA samples used for transcriptome analyses were quantified (Qubit RNA HS Assay, Thermo Fisher Scientific) and quality measured by capillary electrophoresis using the Fragment Analyzer and the ‘Total RNA Standard Sensitivity Assay’ (Agilent Technologies, Inc. Santa Clara, USA). All samples in this study showed high quality RNA Quality Numbers (RQN; mean = 9.9). The library preparation was performed according to the manufacturer’s protocol using the Illumina® ‘TruSeq Stranded mRNA Library Prep Kit’. Briefly, 200 ng total RNA were used for mRNA capturing, fragmentation, the synthesis of cDNA, adapter ligation and library amplification. Bead purified libraries were normalized and finally sequenced on the HiSeq 3000/4000 system (Illumina Inc. San Diego, USA) with a read setup of SR 1x150 bp. The bcl2fastq tool was used to convert the bcl files to fastq files as well for adapter trimming and demultiplexing. Results: Data analyses on fastq files were conducted with CLC Genomics Workbench (version 11.0.1, QIAGEN, Venlo. NL). The reads of all probes were adapter trimmed (Illumina TruSeq) and quality trimmed (using the default parameters: bases below Q13 were trimmed from the end of the reads, ambiguous nucleotides maximal 2). Mapping was done against the Mus musculus (mm10; GRCm38.86) (March 24, 2017) genome sequence. After grouping of samples (three biological replicates each) according to their respective experimental condition, multi-group comparisons were made and statistically determined using edgeR on usegalaxy.org The Resulting values were corrected for multiple testing by FDR. A value of ≤0.05 was considered significant. Conclusions: Our study represents the first detailed analysis of Batf-dependent gene expression in naive and activated pDC transcriptomes in a longitduinal study. Our results show that Batf absence significantly altered the global gene expression patterns in pDCs, modulating many biological pathways important for cell development and effector function.
2021-04-01 | GSE170750 | GEO