Comparison of Trail+/+ versus Trail-/- splenic NK cells from naïve and LCMV-infected mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB30459 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3013400.fastq.gz | Fastqsanger.gz | |||
| ERR3013401.fastq.gz | Fastqsanger.gz | |||
| ERR3013402.fastq.gz | Fastqsanger.gz | |||
| ERR3013403.fastq.gz | Fastqsanger.gz | |||
| ERR3013394.fastq.gz | Fastqsanger.gz |
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Project description:Investigation of the change of the Trail-dependent NK cell transcriptome during short-term (24h) infection with lymphocytic choriomeningitis virus (LCMV). RNA sequencing-based transcriptomics analysis was performed in spleen-isolated (NK1.1+CD3-) NK cells from 3 naïve Trail+/+ mice, 3 naive Trail-/- mice, 4 LCMV-infected Trail+/+ mice, and 4 LCMV-infected Trail-/- mice.
2019-08-27 | E-MTAB-7562 | biostudies-arrayexpress
Project description:Comparison of Trail+/+ versus Trail-/- splenic NK cells from naïve and LCMV-infected mice
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Project description:Infection with acute and chronic strains of LCMV (Armstrong (ARM) and Clone 13 (C13), respectively) leads to massive proliferation of monocytic cells contemporaneously with peak of the anti-viral CD8+ T cell response. These cells return to naïve levels following ARM infection. However, during C13 infection these cells are sustained at high levels and gain a T cell suppressive function at day 14 post infection. The mechanisms by which these cells are induced to proliferate and impair T cell function during chronic LCMV infection are largely unknown. To address this, we analyzed gene expression profiles using microarray analysis of purified splenic monocytic cells (CD11b+ Ly6Chi Gr-1low) from naïve mice, or day 14 LCMV ARM or LCMV C13 infected mice.
2013-02-25 | GSE43896 | GEO
Project description:To identify mechanisms behind immunosuppression during virus infections, we infected mice with LCMV-Armstrong and LCMV-Clone 13 expression patterns. LCMV-Armstrong induces a T-cell reaction that resolves infection within 8-10 days, while LCMV-Clone13 generates a persisten infection through immunosuppression. We used microarray to uncover splenic gene expression patterns specific to each LCMV infection at 5, 9, and 30 days C57BL6 mice, 6-10 weeks old, were infected with LCMV-Armstrong and LCMV-Clone 13 or left uninfected (naïve). At days 5, 9, and 30 whole spleens were harvested for RNA extraction and hybridization on Affymetric microarray.
2013-02-15 | E-GEOD-44322 | biostudies-arrayexpress
Project description:The co-infection of hepatitis B (HBV) patients with the hepatitis D virus (HDV) causes the most severe form of viral hepatitis and thus drastically worsens the course of the disease. Therapy options for HBV/HDV patients are still limited. Here, we investigated the potential of natural killer (NK) cells that are crucial drivers of the innate immune response against viruses to target HDV-infected hepatocytes. We established in vitro co-culture models using HDV-infected hepatoma cell lines and human peripheral blood NK cells. We determined NK cell activation by flow cytometry, transcriptome analysis, bead-based cytokine immunoassays, and NK cell-mediated effects on T cells by flow cytometry. We validated the mechanisms using CRISPR/Cas9-mediated gene deletions. Moreover, we assessed the frequencies and phenotype of NK cells in peripheral blood of HBV and HDV superinfected patients. Upon co-culture with HDV-infected hepatic cell lines, NK cells upregulated activation markers, interferon-stimulated genes (ISGs) including the death receptor ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), produced interferon (IFN)-gamma and eliminated HDV-infected cells via the TRAIL-TRAIL-R2 axis. We identified IFN-beta released by HDV-infected cells as an important enhancer of NK cell activity. In line with our in vitro data, we observed activation of peripheral blood NK cells from HBV/HDV co-infected, but not HBV mono-infected patients. Our data demonstrate NK cell activation in HDV infection and their potential to eliminate HDV-infected hepatoma cells via the TRAIL/TRAIL-R2 axis which implies a high relevance of NK cells for the design of novel anti-viral therapies.
2023-12-04 | GSE249240 | GEO
Project description:Splenic LCMV-specific B cells in acute versus chronic LCMV infection
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Project description:We report the transcriptome of subsets of mouse splenic mesenchymal reticular cells and lymph node reticular cells obtained from healthy Ccl19-cre x R26R-EYFP mice on a C57BL/6 background. We also examine splenic reticular cells from these mice infected with lymphocytic choriomeningitis virus (LCMV) strain Armstrong (acute infection) or strain Clone 13 (chronic infection). Subsets of CD45- CD31- Ter119- reticular cells were analyzed including PDPN+ T zone reticular cells (TRC) and MAdCAM-1+ marginal reticular cells (MRC) from spleen and lymph nodes. Additionally from the spleen we analyzed PDPN+ CD140a- cells, PDPN+ EYFP- cells, and EYFP+ red pulp reticular cells (RPRC) in healthy mice. We analyzed TRC, MRC, PDPN+ EYFP- cells, and EYFP+ RPRC from mice infected with LCMV Armstrong or LCMV Clone-13 on day 8 or on day 30 after infection. Our study represents the first detailed analysis of splenic reticular cell transcriptomes in healthy and LCMV-infected mice, with biologic replicates, generated by RNA-sequencing. We find substantial differential gene expression across subsets of splenic and lymph node reticular cells. We reveal significant changes in gene expression induced after virus infection that differ markedly with disease.
2022-01-09 | GSE171124 | GEO
Project description:NK cells may provide a “rheostat” function and have been shown to reduce the magnitude of antigen-specific T cell responses following infection. It remains unknown whether NK cells similarly modulate vaccine-elicited T cell responses following viral challenge. We used the LCMV clone 13 infection model to address whether NK cells regulate T cell responses in Adenovirus vector vaccinated mice following challenge. As expected, NK cell depletion in unvaccinated mice resulted in increased virus-specific CD4+ and CD8+ T cell responses and immunopathology following LCMV challenge. In contrast, NK cell depletion had minimal to no impact on antigen-specific T cell responses in mice that were vaccinated with an Ad5-GP vector prior to LCMV challenge. Moreover, NK cell depletion in vaccinated mice prior to challenge did not result in immunopathology and did not compromise protective efficacy. These data suggest that Adenovirus vaccine-elicited T cells may be less sensitive to NK cell-rheostat regulation than are T cells primed by LCMV infection.
2018-01-10 | GSE107116 | GEO
Project description:ChIP-seq was conducted using freshly isolated (resting) splenic WT NK cells with anti-Runx3 antibody (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control. Runx3 and H3K4me1 IP from splenic NK cells isolated by negative selection using NK cell isolation kit (R&D) followed by sorting of NKp46+ cells.
2013-11-18 | E-GEOD-50127 | biostudies-arrayexpress
Project description:Purpose: To elucidate the potential immune-regulatory mechanism of TRAIL of activated T cells in EAE, we analyzed gene expression profiles of splenic CD4+ T cells from EAE mice treated with TRAIL by RNA sequencing and transcriptome analysis. Methods: Splenic CD4+ T cell mRNA profiles of control or EAE mice treated with vehicle or TRAIL were generated by deep sequencing using Illumina Solexa. Library construction of all samples were used by Agilent's SureSelect Strand Specific RNA Library Preparation Kit for 75SE (Single-End or Paired-End) sequencing on Solexa platform. The sequence was directly determined using sequencing-by-synthesis technology via the TruSeq SBS Kit. Raw sequences were obtained from the Illumina Pipeline software bcl2fastq v2.0 and expected to generate 20M (million reads or Gb) per sample. Results: By comparing mRNA exression of splenic CD4+ T cells from EAE mice treated with vehicle or TRAIL, there were 244 genes significantly differentially expressed. By analyzing these 244 significant genes categorized by a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the most significantly enriched category for CD4+ T cells was “cell cycle” (multiple of enrichment: 3.13, p = 1.64 × 10−5) followed by “TCR signaling pathway” (multiple of enrichment: 2.80, p = 8.25 × 10−4). In addition, significant genes in the“TCR signaling pathway” tended to be downregulated while those in “cell cycle”tended to be upregulated in a volcano plot analysis. Consistent with the volcano plot results, by using unsupervised hierarchical clustering, the heatmap showed that significant TCR signaling pathway-associated genes were downregulated, while significant cell cycle-associated genes were upregulated in splenic CD4+ T cells from EAE mice treated with TRAIL Conclusions: Our study demonstrated the gene transcription pattern from CD4+ T cells of TRAIL-treated EAE mice were involved in distinct TCR signaling and cell cycle pathways.
2017-12-27 | GSE108523 | GEO