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MiRNA profiles of tonsillar B cell subsets

ABSTRACT: 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.

ORGANISM(S): Human gammaherpesvirus 8 Mus musculus JC polyomavirus Rattus norvegicus Betapolyomavirus macacae Homo sapiens Murid gammaherpesvirus 4 Human immunodeficiency virus 1 Human betaherpesvirus 5 Betapolyomavirus hominis Human alphaherpesvirus 1 human gammaherpesvirus 4 Murid betaherpesvirus 1

PROVIDER: GSE27504 | GEO | 2011/02/25

SECONDARY ACCESSION(S): PRJNA138585

REPOSITORIES: GEO

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miRNA profiles of tonsillar B cell subsets

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

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microRNA expression in human tonsillar B cell populations

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2010-07-23 | E-GEOD-23090 | biostudies-arrayexpress

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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.

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microRNA expression in human tonsillar B cell populations

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DNA Methyltransferase 1 and DNA Methylation Patterning Contribute to Germinal Center B-Cell Differentiation

Project description:We performed DNA methylation (HELP) and gene expression profiling in 17 samples of purified Germinal center B cells (GCBs) and Naive B cells (NBC). We performed supervised analysis using HELP data and defined DNA methylation signature differentiting 2 subgroups of B cvells. Study included purification of human B cells form reactive tonsils, DNA purification and DNA methylation analysis using HELP assay.

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DNA Methylation Dynamics of Germinal Center B Cells Are Mediated by AID

Project description:Changes in DNA methylation are required for the formation of germinal centers (GC), but the mechanisms of such changes are poorly understood. Activation-induced cytidine deaminase (AID) has been recently implicated recently in DNA demethylation through its deaminase activity coupled with DNA repair. We investigated the epigenetic function of AID in vivo in germinal center B cells (GCB) isolated from wild type (WT) and AID-deficient (Aicda-/-) mice. We determined that the transit of B cells through the GC is associated with marked locus-specific loss of methylation and increased methylation diversity, both of which are lost in Aicda-/- animals. Differentially methylated cytosines (DMCs) between GCB and naïve B cells (NB) are enriched in genes that are targeted for somatic hypermutation (SHM) by AID and these genes form networks required for B cell development and proliferation. Finally, we observed significant conservation of AID-dependent epigenetic reprogramming between mouse and human B cells. ERRBS and RNA-seq of wild type and Aicda knockout murine naive and germinal center B cells. ERRBS of human naive and germinal center B cells

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