MicroRNA expression in human tonsillar B cell populations
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE23090 | GEO | 2010/07/24
SECONDARY ACCESSION(S): PRJNA131879
REPOSITORIES: GEO
Similar Datasets
Project description:small RNA profiles of 6 human tonsillar B cell populatios (naive B cells, pre-germinal center B cells, centrocytes, centroblasts, memory B cells, and plasma cells) were determined by deep sequencing. These samples were compared to mouse developing lymphocytes, various hematopoietic cell lineages, and tissues. small RNA expression profiles of 6 well defined B cell populations isolated from human tonsils.
2010-07-23 | E-GEOD-23090 | biostudies-arrayexpress
Project description:In order to assess the miRNA signature of B cells undergoing the germinal center reaction, we isolated three subsets of B cells from tonsils--naive (N), germinal center (GC), and memory (M) and looked at their miRNA profile. We looked at three subsets of B cells, isolated from tonsils obtained from four different donors. Thus, we profiled a total of 12 samples, and each tonsillar subset--N, GC, and M, had four biological replicates.
2011-02-25 | E-GEOD-27504 | biostudies-arrayexpress
Project description:ATAC-seq in sorted GC centroblasts (GCB: CD20+CD44-CD10+CXCR4+), GC centrocytes (CC: CD20+CD44-CD10+CXCR4-), naïve B cells (NB: CD20+CD44+CD10-IgD+), memory B cells (MB: CD20+CD44+CD10-CD38-CD27+), and plasma cells (PC: CD20+CD44+CD10-CD38+CD27+)
2021-08-03 | GSE159314 | GEO
Project description:In order to assess the miRNA signature of B cells undergoing the germinal center reaction, we isolated three subsets of B cells from tonsils--naive (N), germinal center (GC), and memory (M) and looked at their miRNA profile.
2011-02-25 | GSE27504 | GEO
Project description:BFL-1 is an understudied anti-apoptotic protein that is upregulated in melanoma, certain forms of leukemias and lymphomas, and Epstein-Barr virus (EBV)-immortalized lymphoblastoid cell lines (LCLs). We have previously shown that BFL-1 is upregulated in LCLs through a viral-mediated chromatin conformation. However, BFL-1 is also highly expressed in uninfected B cells undergoing maturation in the germinal center. We therefore sought to determine the non-viral mechanisms underlying BFL-1 upregulation in B cells. Here, we characterized the chromatin landscape of maturing B cell subsets found in human tonsillar lymphoid tissue. While chromatin accessibility at the BFL-1 locus increases as naïve B cells enter the germinal center reaction, we found that BFL-1 expression during the transition from dark zone to light zone correlates with a significant increase in three-dimensional chromatin association between upstream enhancer regions and the BFL-1 transcriptional start site (TSS). Interestingly, both LCLs and germinal center light zone B cells shared similar chromatin architectures at the BFL-1 TSS, suggesting a conserved mechanism underlying BFL-1 upregulation. Increased BFL-1 in LCLs also protects against FasL and TRAIL-activated extrinsic apoptosis. In addition to BFL-1 expression, LCLs and germinal center light zone B cells share similar patterns of gene expression, suggesting strong evidence that EBV infection phenocopies various aspects of the germinal center reaction. From this, we infer that EBV-infected B cells co-opts strategies from germinal center light zone B cells to upregulate BFL-1 and enhance their survival in establishing long-lived latent infection.
2020-10-21 | GSE159674 | GEO
Project description:Hodgkin lymphoma is derived from germinal center / post-germinal center B cells. Gene expression profilies of the Hodgkin lymphoma cell lines were compared to 5 samples of CD77+ centroblasts derived from reactive tonsils
2012-08-31 | E-GEOD-39132 | biostudies-arrayexpress
Project description:Whole genome gene expression microarrays made it possible to pick up genes, whose products could be involved in a biological pathway. The aim of this study is to provide easy tools to interrogate whole genome transcriptome changes in the process of plasma cell generation, starting from naive B cells and comprising centroblasts, centrocytes, memory B cells, preplasmablasts, plasmablasts, early plasma cells, and mature bone marrow plasma cells.
2013-07-10 | E-MTAB-1771 | biostudies-arrayexpress
Project description:ATAC-seq in murine naive B cells, germinal center B cells, and total B cells stimulated with LPS ex vivo and transduced with empty vector or Ocab (Pou2af1) expression vector.
2023-10-13 | GSE245298 | GEO
Project description:We used Cd19-Cre to conditionally delete Hdac3 in order to define its role in germinal center B cells, which represent the cell of origin for many B cell malignancies. Cd19-Cre-Hdac3-/- mice showed impaired germinal center (GC) formation along with a defect in plasmablast generation. Analysis of Hdac3-/- GCs revealed a reduction in dark zone centroblasts and accumulation of light zone centrocytes. RNA-seq revealed a significant correlation between genes up-regulated upon Hdac3 loss and those up-regulated in Foxo1-deleted GC B cells, even though Foxo1 typically activates transcription. Therefore, to determine whether gene expression changes observed in Hdac3-/- GCs were a result of direct effects of Hdac3 deacetylase activity on transcription, we used an HDAC3 selective inhibitor to examine nascent transcription in germinal center-derived cell lines. Transcriptional changes upon HDAC3 inhibition in cells highly correlated with transcriptional changes observed in GCs in vivo. Further comparison of PRO-seq data with ChIP-seq/exo data for BCL6, SMRT, FOXO1 and H3K27ac identified direct targets of HDAC3 function including CD86, CD83 and CXCR5 that are likely responsible for driving the light zone phenotype observed in vivo.
2019-09-12 | GSE130516 | GEO
Project description:We used Cd19-Cre to conditionally delete Hdac3 in order to define its role in germinal center B cells, which represent the cell of origin for many B cell malignancies. Cd19-Cre-Hdac3-/- mice showed impaired germinal center (GC) formation along with a defect in plasmablast generation. Analysis of Hdac3-/- GCs revealed a reduction in dark zone centroblasts and accumulation of light zone centrocytes. RNA-seq revealed a significant correlation between genes up-regulated upon Hdac3 loss and those up-regulated in Foxo1-deleted GC B cells, even though Foxo1 typically activates transcription. Therefore, to determine whether gene expression changes observed in Hdac3-/- GCs were a result of direct effects of Hdac3 deacetylase activity on transcription, we used an HDAC3 selective inhibitor to examine nascent transcription in germinal center-derived cell lines. Transcriptional changes upon HDAC3 inhibition in cells highly correlated with transcriptional changes observed in GCs in vivo. Further comparison of PRO-seq data with ChIP-seq/exo data for BCL6, SMRT, FOXO1 and H3K27ac identified direct targets of HDAC3 function including CD86, CD83 and CXCR5 that are likely responsible for driving the light zone phenotype observed in vivo.
2019-09-12 | GSE130502 | GEO