Transcriptome profile of GEN2.2 cell line after CpG stimulation
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE59887 | GEO | 2014/07/30
SECONDARY ACCESSION(S): PRJNA256990
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of expression profile of human GEN2.2 cell line RNA expression profile of the human pDC cell line GEN2.2 Total RNA was isolated from GEN2.2 cells growing at log phase with High Pure RNA isolation Kit (Roche Diagnostics, Mannheim, Germany), according with the manufacturer´s instructions in quintuplicate. A total of 300 ng of total RNA was processed using Illumina TotalPrep RNA Amplification Kit. Hybridization of human samples was performed on Illumina Human-HT12 Version 4.
2014-07-30 | E-GEOD-59887 | biostudies-arrayexpress
Project description:Transcriptome profile of GEN2.2 cell line after CpG stimulation
| PRJNA256990 | ENA
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. Keywords: time course
2007-12-13 | GSE7831 | GEO
Project description:Analysis of expression profile of human GEN2.2 shSIDT1 cell line and their controls cultured in the presence of ODN2006 for different time points.
2019-01-11 | GSE124941 | 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: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
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.
2016-11-30 | GSE70276 | GEO
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.
2016-11-30 | GSE70275 | GEO
Project description:RNAseq was performed to understand the role of SMRT in CD8α+ DCs. MutuDC cell line was transduced with empty and smrt shrna lentiviral particles and cells were prepared in unstimulated or 6hr CpG stimulation condition.
2022-09-20 | E-MTAB-10864 | biostudies-arrayexpress
Project description:RNAseq were performed to understand the role of SMRT in CD8α+ DCs. MutuDC line were transduced with empty vector and SMRT shRNA using lentivirus and cells were prepared in unstimulated or 6hr CpG stimulation condition.
2022-09-20 | E-MTAB-10070 | biostudies-arrayexpress