Transcriptome profiling of dendritic cells during JEV infection
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE160178 | GEO | 2021/07/07
REPOSITORIES: GEO
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Project description:Transcriptome profiling of dendritic cells during JEV infection
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Project description:A growing body of evidence suggests that inflammatory cytokines have a dualistic role in immunity. In this study, we sought to determine the direct effects IFN-gamma on the differentiation and maturation of human peripheral blood monocyte-derived dendritic cells (moDC). Here, we report that following differentiation of human peripheral-blood monocytes into moDCs with granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-4, interferon-gamma (IFN-gamma) induces moDC maturation and up-regulates the co-stimulatory markers CD80, CD86, CD95, and MHC Class I, enabling moDCs to effectively generate antigen-specific CD4+ and CD8+ T cell responses for multiple viral and tumor antigens. Interestingly, early exposure of monocytes to high concentrations of IFN-gamma promotes monocyte differentiation into macrophages, despite the presence of GM-CSF and IL-4. However, under low concentrations of IFN-gamma, monocytes continue to differentiate into dendritic cells possessing a unique gene-expression profile, resulting in impairments in subsequent maturation by IFN-gamma and an inability to generate effective antigen-specific CD4+ and CD8+ T cell responses compared to standard moDCs. Monocytes differentiated in the presence of low levels of IFN-gamma downregulate IFN-gamma receptor expression, impairing their response to an inflammatory rechallenge. These findings demonstrate the ability of IFN-gamma to impart differential programs on human moDCs which shape the antigen-specific T cell responses they induce. Timing and intensity of exposure to IFN-gamma can thus determine whether moDCs are tolerogenic or immunostimulating. Human monocyte-derived dendritic cells from 4 healthy donors were differentiated with either GM-CSF and IL-4 (n=4) or GM-CSF, IL-4, and IFN-gamma (n=4). These samples were subsequently hybridized to arrays as 4 biological repeats for each of the two treatment conditions.
2014-06-01 | E-GEOD-47621 | biostudies-arrayexpress
Project description:Infection by neurotropic virus Japanese Encephalitis Virus (JEV) is characterized by profound neuronal cell death and neuroinflammation. Long non-coding RNAs (lncRNAs) are critical regulatory players in diverse biological processes, including viral pathogenesis. We use whole transcriptomic sequencing to identify a lncRNA JINR1 (JEV-induced non-coding RNA 1) induced upon JEV infection in neuronal cells. Transcription factor NF-κB triggers JINR-1 expression during JEV infection. Loss of JINR-1 impairs virus replication and reduces JEV-induced neuronal cell death and expression of genes involved in ER stress and neuroinflammation. Mechanistically, JINR1 inhibits the expression of mir-216-5p, which inhibits host factors GRP78 and c-JUN and the viral genome. In line with its role as a pro-viral host factor, JINR1 interacts with RBM10 and NF-κB to promote the expression of genes involved in ER stress and neuroinflammation. Our results suggest a role for JINR-1 in promoting JEV-induced cell death and neuroinflammation.
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2020-01-07 | GSE143143 | GEO
Project description:A growing body of evidence suggests that inflammatory cytokines have a dualistic role in immunity. In this study, we sought to determine the direct effects IFN-gamma on the differentiation and maturation of human peripheral blood monocyte-derived dendritic cells (moDC). Here, we report that following differentiation of human peripheral-blood monocytes into moDCs with granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-4, interferon-gamma (IFN-gamma) induces moDC maturation and up-regulates the co-stimulatory markers CD80, CD86, CD95, and MHC Class I, enabling moDCs to effectively generate antigen-specific CD4+ and CD8+ T cell responses for multiple viral and tumor antigens. Interestingly, early exposure of monocytes to high concentrations of IFN-gamma promotes monocyte differentiation into macrophages, despite the presence of GM-CSF and IL-4. However, under low concentrations of IFN-gamma, monocytes continue to differentiate into dendritic cells possessing a unique gene-expression profile, resulting in impairments in subsequent maturation by IFN-gamma and an inability to generate effective antigen-specific CD4+ and CD8+ T cell responses compared to standard moDCs. Monocytes differentiated in the presence of low levels of IFN-gamma downregulate IFN-gamma receptor expression, impairing their response to an inflammatory rechallenge. These findings demonstrate the ability of IFN-gamma to impart differential programs on human moDCs which shape the antigen-specific T cell responses they induce. Timing and intensity of exposure to IFN-gamma can thus determine whether moDCs are tolerogenic or immunostimulating.
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Project description:B16F10, a murine melanoma cel line is cytolytic to JEV infection. We have identified a B16F10 cell line variant which is non-cytolytic to JEV infection. This variant cell line has two types of cells, one which is persistently infected JEV and another which is resistant to JEV infection. The JEV-resistant cells (B16F10r) were seperated from the presistently infected cells by single cell cloning. To understand the mechanism of JEV resistance microarray analysis was caried out to Identify and characterize genes differentially expressed during in uninfected/JEV-infected B16F10 and B16F10r cells. Agilent one-color experiment,Organism: Mus musculus ,Agilent Custom Mouse Whole Genome Mouse 8x60k Gene expression designed by Genotypic Technology Private Limited, Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
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Project description:B16F10, a murine melanoma cel line is cytolytic to JEV infection. We have identified a B16F10 cell line variant which is non-cytolytic to JEV infection. This variant cell line has two types of cells, one which is persistently infected JEV and another which is resistant to JEV infection. The JEV-resistant cells (B16F10r) were seperated from the presistently infected cells by single cell cloning. To understand the mechanism of JEV resistance microarray analysis was caried out to Identify and characterize genes differentially expressed during in uninfected/JEV-infected B16F10 and B16F10r cells.
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