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Gene expression data from murine mDC and pDC

ABSTRACT: mDC and pDC exhibit distinct TLR expression pattern and differ in their responses to various TLR ligands. The goal of this study was to identify genes, that were differentally expressed between mDC and pDC as a means to determine how TLR signaling pathways operate. Suprisingly, expression of TLR-assoociated signaling proteins were found to be present at equivalent levels between mDC and pDC, despite differential expression of TLRs, and thus revealing insight into use of adaptor proteins that function as general regulators of TLR signaling pathways in both cell types. mDC and pDC were sorted from spleens of mice in 2 independent experiments: The first experiment included 2 replicates of pDC that were cultured in medium for 1h prior to RNA extraction and 1 replicate of mDC that were directly processed for RNA extraction after the sort. In a second experiment we obtained 2 more replicates of mDC that were processed for RNA extraction directly after the sort and run on a seperate microarray for gene expression analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Amaya Wolf

PROVIDER: E-GEOD-50436 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression data from murine mDC and pDC

Project description:mDC and pDC exhibit distinct TLR expression pattern and differ in their responses to various TLR ligands. The goal of this study was to identify genes, that were differentally expressed between mDC and pDC as a means to determine how TLR signaling pathways operate. Suprisingly, expression of TLR-assoociated signaling proteins were found to be present at equivalent levels between mDC and pDC, despite differential expression of TLRs, and thus revealing insight into use of adaptor proteins that function as general regulators of TLR signaling pathways in both cell types.

2014-01-01 | GSE50436 | GEO

Transcription profiling of mouse immature pDC and pDC activated with CpG 1826 and influenza virus PR8

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 Âµg/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

Expression data from immature pDC and pDC activated with CpG 1826 and influenza virus PR8

2007-12-13 | GSE7831 | GEO

Dissecting cell-intrinsic roles of MyD88 and IFN-I signalling in pDC responses to a viral infection in vivo

Project description:Plasmacytoid dendritic cells (pDC) are the major source of type I interferons (IFN-I) during viral infections, in response to triggering of endosomal Toll Like Receptors (TLR) 7 or 9 by viral single-stranded RNA or unmethylated CpG DNA, respectively. IFN-I production in pDC occurs in specialized endosomes encompassing preformed signaling complexes of TLR7 or 9 with their adaptor molecule MyD88 and the transcription factor interferon regulatory factor 7 (IRF7). The triggering of TLR leads to IRF7 phosphorylation, nuclear translocation and binding to the promoters of the genes encoding IFN-I to initiate their transcription. pDC express uniquely high levels of IRF7 at steady state and this expression is further enhanced by positive IFN-I feedback signaling during viral infections. However, the specific cell-intrinsic roles of MyD88 versus IFN-I signaling in pDC responses to a viral infection have not been rigorously dissected. To achieve this aim, we generated mixed bone marrow chimera mice (MBMC) allowing to rigorously compare the gene expression profiles of WT versus Ifnar1-KO or MyD88-KO pDC isolated from the same animals at steady state or after infection with the mouse cytomegalovirus (MCMV). Our results indicate that, in vivo during MCMV infection, pDC undergo a major transcriptional reprogramming, under combined instruction of IFN-I, IFN-γ and direct TLR triggering. However, these different stimuli drive specific, largely distinct, gene expression programs. We rigorously determined which gene modules require cell-intrinsic IFN-I signaling for their induction in pDC during a physiological viral infection in vivo. We delineated non-redundant versus shared versus antagonistic responses with IFN-γ. We demonstrated that cell-intrinsic IFN-I responsiveness is dispensable for induction of the expression of all IFN-I/III genes and many cytokines or chemokines in pDC during MCMV infection, contrary to MyD88 signaling.

2018-10-05 | GSE107876 | GEO

Gene profiling for B cells and B cells from pDC coculture system in response to R848 stimulation

Project description:Transcriptomic analysis revealed that IFN-I and Mapk pp38 signaing were found to be critical for the pDC-enhanced TLR-mediated B cell responses.

2021-05-21 | GSE174755 | GEO

mRNA expression analysis of several cell subset from peripheral blood of SLE patient and Healthy Control

Project description:Isolated T, B, monocyte, mDC, pDC, naiveB, memoryB and PBMC at spontaneous state from peripheral blood

2022-09-26 | GSE148601 | GEO

Transcriptional repression of IRF7 by MYC is critical for antiviral immune response in human pDC [pDC]

Project description:Type I interferons (IFN) are crucial mediators of human innate and adaptive immunity and are massively produced from plasmacytoid dendritic cells (pDC). IRF7 is a critical regulator of type I IFN production when pathogens are detected by TLR7/9 in pDC. However, hyperactivation of pDC can cause life-threatening autoimmune diseases. To avoid the deleterious effects of aberrant pDC activation, tight regulation of IRF7 is required. Nonetheless, the detailed mechanisms of how IRF7 transcription is regulated in pDC are still elusive. To this end, we identified the global gene expression changes after stimulation of human primary pDC with the TLR9 agonist CpGB. We identified that the transcription factor MYC is prominently upregulated upon CpGB engagement in pDC. Moreover, when we knocked down MYC in the pDC-like cell line GEN2.2, production of interferon-stimulated genes (ISGs) was dramatically increased and was further enhanced by CpGB. Interestingly, MYC is shown to be recruited to the IRF7 promoter region through interaction with NCOR2/HDAC3 for its repression, and HDAC3 inhibition enhanced IRF7 expression and IFNβ production. Interestingly, activation of TLR9-mediated NF-kB and MAPK and nuclear translocation of IRF7 were greatly enhanced by MYC depletion. Pharmaceutical inhibition of MYC recovered IRF7 expression, further confirming the negative role of MYC in the antiviral response by pDC. Furthermore, the inverse correlation of MYC and IRF7 was validated in psoriasis skin sample datasets. Therefore, our results identify the novel immunomodulatory role of MYC in human pDC and may add to our understanding of aberrant pDC function in autoimmune diseases.

2018-06-01 | GSE70277 | GEO

Expression data from pDC infected with Aspergillus fumigatus

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 FcRÎ³ 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

microRNA changes during Dex-induced pDC apoptosis

Project description:To identify microRNA changed during Dex-induced pDC apoptosis and CpG hampered Dex-induced pDC apoptosis

2016-04-20 | GSE46445 | GEO

Sca-1 expression defines different developmental stages of mouse PDC that show functional heterogeneity in the endosomal but not lysosomal TLR9 response

Project description:Plasmacytoid dendritic cells (PDC) play an important role in innate and adaptive immunity and were shown to be identical to previously described natural IFN-M-NM-1-producing cells (NIP). Here, we describe two functionally distinct PDC subpopulations that are characterized by the differential expression of stem cell antigen-1 (Sca-1; Ly-6A/E). Sca-1- PDC are mainly found in the bone marrow, appear first during development, show a higher proliferative activity and represent the more precursor phenotype. Sca-1+ PDC are mostly located in secondary lymphoid organs and show higher expression of MHC class II molecules. Sca-1- PDC give rise to a Sca-1+ subset upon activation or in response to tissue-specific factors. Interestingly, in contrast to Sca-1- PDC, Sca-1+ PDC are defective in type I IFN production upon endosomal TLR9 stimulation, whereas lysosomal signaling via TLR9 is functional in both subsets. Gene expression analysis revealed that osteopontin (Opn) is strongly upregulated in Sca-1- PDC. This data provides evidence for the molecular basis of the observed functional heterogeneity, as the intracellular isoform of Opn couples TLR9 signaling to IFN-M-NM-1 expression. Taken together, our results indicate that Sca-1- PDC are an early developmental stage of PDC with distinct innate functions representing the true murine NIP. The dataset comprises eight samples divided into two sample groups consisting of Sca-1(-) and Sca-1(+) PDCs collected from in vitro culture of differentiated bone marrow precursor cells using mFlt3-L

2013-12-21 | E-GEOD-42860 | biostudies-arrayexpress

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