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Molecular control of myeloid suppressors by death pathways

ABSTRACT: The goal of this study was to evaluate the mechanisms distinguishing the different forms of myeloid suppressors in cancer and inflammation, and their indivdual roles in T cell suppression

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE61479 | GEO | 2015/04/28

SECONDARY ACCESSION(S): PRJNA261278

REPOSITORIES: GEO

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Molecular control of myeloid suppressors by death pathways

Project description:The goal of this study was to evaluate the mechanisms distinguishing the different forms of myeloid suppressors in cancer and inflammation, and their indivdual roles in T cell suppression We used microarrays to profile the expression profile of myeloid suppressor cells in mouse and human samples. The starting point is the attached arrays which use different CD11+ or CD14+ selections to crudely separate the myeloid suppressors from other immune cells. The overall study is an initial step towards much higher resolution genetics studies to determine the functional prathways used by myeloid suppressors to inhibit T-cells.

2015-04-28 | E-GEOD-61479 | biostudies-arrayexpress

Molecular control of myeloid suppressors by death pathways

Project description:Molecular control of myeloid suppressors by death pathways

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TaqMan Peripheral blood mononuclear cell miRNA profiles of HIV-1-infected elite suppressors, viremic patients, and uninfected control donors

Project description:This study used TaqMan low-density arrays to identify and quantitate circulating cellular miRNAs during HIV-1 elite suppression, active HIV-1 replication, and uninfected status. Blood samples were from six uninfected controls, six HIV-1 elite suppressors with undetectable viral load, and six viremic HIV-1-infected patients.

2012-02-22 | E-GEOD-33492 | biostudies-arrayexpress

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Project description:This study used the NanoString nCounter hybridization system and nCounter miRNA expression assays to identify and quantitate circulating cellular miRNAs during HIV-1 elite suppression, active HIV-1 replication, and uninfected status. Blood samples were from eight uninfected controls, seven HIV-1 elite suppressors with undetectable viral load, and six viremic HIV-1-infected patients.

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Mouse cytomegalovirus M36 and M45 death suppressors cooperate to prevent inflammation resulting from antiviral programmed cell death pathways.

Project description:The complex interplay between caspase-8 and receptor-interacting protein (RIP) kinase RIP 3 (RIPK3) driving extrinsic apoptosis and necroptosis is not fully understood. Murine cytomegalovirus triggers both apoptosis and necroptosis in infected cells; however, encoded inhibitors of caspase-8 activity (M36) and RIP3 signaling (M45) suppress these antiviral responses. Here, we report that this virus activates caspase-8 in macrophages to trigger apoptosis that gives rise to secondary necroptosis. Infection with double-mutant ΔM36/M45mutRHIM virus reveals a signaling pattern in which caspase-8 activates caspase-3 to drive apoptosis with subsequent RIP3-dependent activation of mixed lineage kinase domain-like (MLKL) leading to necroptosis. This combined cell death signaling is highly inflammatory, greater than either apoptosis induced by ΔM36 or necroptosis induced by M45mutRHIM virus. IL-6 production by macrophages is dramatically increased during double-mutant virus infection and correlates with faster antiviral responses in the host. Collaboratively, M36 and M45 target caspase-8 and RIP3 pathways together to suppress this proinflammatory cell death. This study reveals the effect of antiviral programmed cell death pathways on inflammation, shows that caspase-8 activation may go hand-in-hand with necroptosis in macrophages, and revises current understanding of independent and collaborative functions of M36 and M45 in blocking apoptotic and necroptotic cell death responses.

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Project description:Several mechanisms have been implicated in MDSC-mediated suppression of immune responses. To better understand the mechanism(s)/pathway(s) MDSCs utilize to suppress immune responses, we performed a transcriptome profiling of CD11b+CD11c+ (good suppressors) and CD11b+CD11c- (poor suppressors) MDSCs. Comparison of the respective transcriptomes allowed us to identify target genes associated with immunosuppression.

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Broad H3K4me3 Reveals Increased Transcription Elongation and Enhancer Activity at Tumor Suppressors

Project description:Tumor suppressors are mostly defined by inactivating somatic mutations in tumors, yet little is known about their epigenetic features in normal cells. Here, through integrative analysis of 1,134 genome-wide epigenetic profiles and mutations from >8,200 tumor-normal pairs, we discovered broad H3K4me3 (wider than 4 kb) as the first epigenetic signature for tumor suppressors in normal cells. Broad H3K4me3 is associated with increased transcription elongation and enhancer activity together leading to exceptionally high gene expression, and is distinct from other broad epigenetic features, such as super enhancers. Broad H3K4me3 conserved across normal cells represents core tumor suppressors, such as P53 and PTEN, whereas cell-type-specific broad H3K4me3 may indicate cell-identity genes and cell-type-specific tumor suppressors. Furthermore, widespread shortening of broad H3K4me3 in cancers is strongly associated with repression of tumor suppressors. Together, the broad H3K4me3 epigenetic signature we reported here may provide a new direction for the discovery and characterization of novel tumor suppressors. H3K4me3 ChIP-Seq was conducted in 1) liver tumor and matched tissue, 2) lung tumor and matched tissue, 3) cell line A549 grown under normal and flavopiridol treatment conditions.

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Broad H3K4me3 Reveals Increased Transcription Elongation and Enhancer Activity at Tumor Suppressors

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