About: Induction of Interferon-Stimulated Genes on the IL-4 Response Axis by Epstein-Barr Virus Infected Human B Cells; Relevance to Cellular Transformation

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About: Induction of Interferon-Stimulated Genes on the IL-4 Response Axis by Epstein-Barr Virus Infected Human B Cells; Relevance to Cellular Transformation Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Induction of Interferon-Stimulated Genes on the IL-4 Response Axis by Epstein-Barr Virus Infected Human B Cells; Relevance to Cellular Transformation
Creator	Smith, N Wei, W Murray, P Tierney, R Vockerodt, M
Source	PMC
abstract	Epstein-Barr virus (EBV) is an oncogenic virus that is associated with the pathogenesis of several human lymphoid malignancies, including Hodgkin's lymphoma. Infection of normal resting B cells with EBV results in activation to lymphoblasts that are phenotypically similar to those generated by physiological stimulation with CD40L plus IL-4. One important difference is that infection leads to the establishment of permanently growing lymphoblastoid cell lines, whereas CD40L/IL-4 blasts have finite proliferation lifespans. To identify early events which might later determine why EBV infected blasts go on to establish transformed cell lines, we performed global transcriptome analyses on resting B cells and on EBV and CD40L/IL-4 blasts after 7 days culture. As anticipated there was considerable overlap in the transcriptomes of the two types of lymphoblasts when compared to the original resting B cells, reflecting common changes associated with lymphocyte activation and proliferation. Of interest to us was a subset of 255 genes that were differentially expressed between EBV and CD40L/IL-4 blasts. Genes which were more highly expressed in EBV blasts were substantially and significantly enriched for a set of interferon-stimulated genes which on further in silico analyses were found to be repressed by IL-4 in other cell contexts and to be up-regulated in micro-dissected malignant cells from Hodgkin's lymphoma biopsies when compared to their normal germinal center cell counterparts. We hypothesized that EBV and IL-4 were targeting and discordantly regulating a common set of genes. This was supported experimentally in our B cell model where IL-4 stimulation partially reversed transcriptional changes which follow EBV infection and it impaired the efficiency of EBV-induced B cell transformation. Taken together, these data suggest that the discordant regulation of interferon and IL-4 pathway genes by EBV that occurs early following infection of B cells has relevance to the development or maintenance of an EBV-associated malignancy.
has issue date	2013-05-27(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0064868
bibo:pmid	23724103
has license	cc-by
sha1sum (hex)	5e0504a1c581c36bbf2c2c97439b87b9834b108b
schema:url	https://doi.org/10.1371/journal.pone.0064868
resource representing a document's title	Induction of Interferon-Stimulated Genes on the IL-4 Response Axis by Epstein-Barr Virus Infected Human B Cells; Relevance to Cellular Transformation
has PubMed Central identifier	PMC3664578
has PubMed identifier	23724103
schema:publication	PLoS One
resource representing a document's body	covid:5e0504a1c581c36bbf2c2c97439b87b9834b108b#body_text
is schema:about of	named entity 'transcriptional' named entity 'IL-4' named entity 'lymphoma' named entity 'data' named entity 'B cell' named entity 'lymphocyte activation' named entity 'Response' named entity 'Transformation' covid:arg/5e0504a1c581c36bbf2c2c97439b87b9834b108b named entity 'This' named entity 'virus' named entity 'B cells' named entity 'up-regulated' named entity 'EBV' named entity 'reflecting' named entity 'finite' named entity 'biopsies' named entity 'normal' named entity 'B cells' named entity 'common' named entity 'analyses' named entity 'identify' named entity 'targeting' named entity 'genes' named entity 'EBV' named entity 'leads' named entity 'IL-4' named entity 'proliferation' named entity 'lymphoblastoid' named entity 'common' named entity 'EBV' named entity 'Cellular' named entity 'Genes' named entity 'EBV' named entity 'CD40L' named entity 'EBV' named entity 'Infection' named entity 'CD40L' named entity 'EBV' named entity 'IL-4' named entity 'interferon-stimulated genes' named entity 'CD40L' named entity 'EBV' named entity 'transcriptomes' named entity 'infection' named entity 'EBV' named entity 'Interferon-Stimulated Genes' named entity 'blasts' named entity 'resting' named entity 'fluorescently labelled' named entity 'transcriptional' named entity 'EBV' named entity 'CD40L' named entity 'RT-qPCR' named entity 'gene expression' named entity 'Epstein-Barr virus' named entity 'CD40L' named entity 'up-regulated' named entity 'aetiologically' named entity 'transcriptional' named entity 'IL-4' named entity '0.01' named entity 'transcriptomes' named entity 'oncogene' named entity 'immune response' named entity 'transcriptional' named entity 'IL-4' named entity 'mitogen' named entity 'gene' named entity 'IFN' named entity 'ISGs' named entity 'EBV' named entity 'tumors' named entity 'tumors' named entity 'DNA genome' named entity 'DUSP6' named entity 'up-regulated'

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