Comparison of gene expression of OT-I CD8 T cells after infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Leo Lefrancois
PROVIDER: E-GEOD-20265 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The goal was to examine gene expression after in vivo activation by different vaccine strains of Listeria monocytogenes. Heat killed LM, irradiated LM and live actA- LM were used to immunize mice after transfer of OT-I cells
2010-06-01 | GSE20265 | GEO
Project description:Purpose: RNA-seq analysis of three memory OT-I cell subsets (from a Klrg1-Cre fate reporter mouse model) isolated from the spleen of C57BL/6 mice infected with Listeria monocytogenes. The hypothesis tested in the present study was that KLRG1+ effector CD8 T lymphocytes differentiate into KLRG1- memory CD8 T lymphocytes and provide long-lasting immunity against infectious diseases and malignancies. Methods: Total RNA was obtained from FACS-purified OT-I cell subsets isolated from spleen 104 (experiment 1) and 110 days post infection (experiment 2) with ovalbumin-expressing Listeria monocytogenes (LM-OVA). Results: Using RNA-seq technology, we performed genome-wide transcriptional profiling of three memory OT-I cells (KLRG1+ Reporter+, KLRG1- Reporter+ (exKLRG1) and KLRG1- Reporter-) and identified 36 genes differentially expressed (> 1.5-fold) between exKLRG1 and KLRG1- Reporter- memory OT-I cells, and 132 differentially expressed genes between exKLRG1 and KLRG1+ Reporter+ memory OT-I cells. We then confirmed the expression of 15 genes/molecules by qRT-PCR and/or flow cytometry. Conclusions: Our study represents the first fate mapping analysis of KLRG1+ effector OT-I cells, demonstrates that KLRG1+ effector OT-I cells differentiate into all memory T cell lineages thereby promoting protective immunity. RNA-seq also identified CX3CR1 as a marker of circulating exKLRG1 early memory OT-I cells.
2018-03-01 | GSE110629 | GEO
Project description:Cerebral listeriosis is characterized by neuronal apoptosis and microglial cell activation, but little is known about the bacterial virulence factors involved in this process and how bacterial dissemination is controlled. Here, we show that the cellular target of Listeria monocytogenes (LM) in murine hippocampal cultures is microglia rather than neurons or other glial cells, which are rarely infected. This in vitro model served to demonstrate that infected microglial cells release a soluble factor to the medium responsible for neuronal apoptosis. We investigated the production of this factor in a well-established murine microglia cell model BV2 cells, and compared with J-774 macrophage cells after infection with different LM bacterial mutants. Our purpose was to study in both cell types parameters such as the listericidal capacities, pro-inflammatory cytokines released, and bacterial factors involved in the intracellular cycle. Our data reveal that microglia shows unique features to handle a LM infection. Microglia is three times more permissive for LM intracellular growth than murine macrophages; while producing five times higher levels of pro-inflammatory cytokines IL-6, MCP-1 and TNF-α than macrophages. Using different LM mutants (i.e., LMWT, LM∆LLO, LM∆ActA or LM∆plcB) we conclude that LLO and ActA are not involved in LM proliferation within microglia cells, while they are required for survival within macrophages. Moreover, ActA controls TNF-α production, a cytokine involved in neural apoptosis. Transcriptional differential response of microglia infected with different LM mutants reflected ActA controls the TNF-a signaling pathway through out molecules and chemokines involved in this pathway such as NFkβ, MAPK-1, Ccl2, Ccl3, Ccl4 and CxCl10. The project implies the analysis of two replicates from three different conditions, in total 6 samples: microglia cells non-infected, microglia cells infected with Listeria monocytogenes (LM) wild type (LLO+), microglia cells infected with LM deficient in listeriolysin O (LLO-) and microglia cells infected with LM deficient in ActA (1942). References samples were microglia cells non-infected (NT). Infection with LM was performed for 1 hour, followed by 24 hours in medium with antibiotics to avoid bacterial extracellular growth. Gene expression analysis was performed using Partek Genomics Suite software (version 6.11.0801; Partek). GeneChip data were filtered to remove those probe sets with an intensity raw value close to background levels. Probe sets for each array are pre-processed using RMA. Also, probe sets whose expression change under all experimental conditions was below a threshold, based on the standard desviation of the normalised intensity values, were filtered.
2011-10-02 | E-GEOD-32505 | biostudies-arrayexpress
Project description:Cerebral listeriosis is characterized by neuronal apoptosis and microglial cell activation, but little is known about the bacterial virulence factors involved in this process and how bacterial dissemination is controlled. Here, we show that the cellular target of Listeria monocytogenes (LM) in murine hippocampal cultures is microglia rather than neurons or other glial cells, which are rarely infected. This in vitro model served to demonstrate that infected microglial cells release a soluble factor to the medium responsible for neuronal apoptosis. We investigated the production of this factor in a well-established murine microglia cell model BV2 cells, and compared with J-774 macrophage cells after infection with different LM bacterial mutants. Our purpose was to study in both cell types parameters such as the listericidal capacities, pro-inflammatory cytokines released, and bacterial factors involved in the intracellular cycle. Our data reveal that microglia shows unique features to handle a LM infection. Microglia is three times more permissive for LM intracellular growth than murine macrophages; while producing five times higher levels of pro-inflammatory cytokines IL-6, MCP-1 and TNF-α than macrophages. Using different LM mutants (i.e., LMWT, LM∆LLO, LM∆ActA or LM∆plcB) we conclude that LLO and ActA are not involved in LM proliferation within microglia cells, while they are required for survival within macrophages. Moreover, ActA controls TNF-α production, a cytokine involved in neural apoptosis. Transcriptional differential response of microglia infected with different LM mutants reflected ActA controls the TNF-a signaling pathway through out molecules and chemokines involved in this pathway such as NFkβ, MAPK-1, Ccl2, Ccl3, Ccl4 and CxCl10.
2011-10-03 | GSE32505 | GEO
Project description:Cognate antigen signals control CD8+ T cell priming, expansion size and effector versus memory cell fates, however, it is not clear whether they can also modulate the functional features of memory CD8+ T cells. We observed that OT-I cells that were primed with weak cognate antigen signals incorporate more cytokine signals, leading to a hypothesis that CD8+ T cells that receive weak TCR signals require cytokine signals to form functional memory. Using a previously described mouse model in which IL-2 signaling via its high affinity receptor CD25 is selectively impaired, the “Il2ramut/mut” mouse, we conducted a comparative analysis of gene expression and epigenetic landscape of Il2ramut/mut and WT OT-I memory cells that were primed with strong (Lm-Ova N4) versus weak (Lm-Ova T4). RNA seq data showed that both TCR and IL-2 priming signals have minimal effect on gene expression in resting memory CD8 T cells, but they significantly modify the epigenetic landscape of the memory CD8 T cells. These findings have important contributions to the current understanding of how priming signals program memory CD8 T cells in vivo.
2020-09-30 | GSE152392 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goal of this study is to compare the transcriptome of OT-1 cells during priming (3 days after infection) and during effector phase ( 7 days after infection) in ODC-OVA mice after LCMV-OVA and Lm-OVA infection
2018-05-17 | GSE93805 | GEO
Project description:Purpose: ATAC-seq analysis of naive and three effector OT-I cell subsets (from a Klrg1-Cre fate reporter mouse model) isolated from the spleen of C57BL/6 mice 0 and 8 days post infection with OVA-expressing Listeria monocytogenes. The hypothesis tested in the present study was that chromatin remodeling in KLRG1+ effector CD8 T lymphocytes promotes the differentiation into KLRG1- memory CD8 T lymphocytes that provide long-lasting immunity against infectious diseases and malignancies. Methods: DNA was obtained from 50,000 FACS-purified OT-I cell subsets isolated from spleen 0 and 8 days post infection with ovalbumin-expressing Listeria monocytogenes (LM-OVA) (experiment 3). Results: Using ATAC-seq technology, we analyzed the chromatin accessibility landscape of naive and three effector OT-I cells (KLRG1+ Reporter+, KLRG1- Reporter+ (exKLRG1) and KLRG1- Reporter-). Conclusions: Our study represents the first fate mapping analysis of KLRG1+ effector OT-I cells, demonstrates that KLRG1+ effector OT-I cells differentiate into all memory T cell lineages thereby promoting protective immunity. RNA-seq identified CX3CR1 as a marker of circulating exKLRG1 early memory OT-I cells, and ATAC-seq analysis revealed that chromatin remodeling enabled exKLRG1 memory cells to exhibit both a high cytotoxic and proliferative capacity.
2018-03-01 | GSE110876 | GEO
Project description:Desulfosporosinus sp. OT genome sequencing
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Project description:Pseudomonas alcaligenes OT 69 strain:OT 69 Genome sequencing and assembly
| PRJNA202928 | ENA
Project description:Cognate antigen signals control CD8+ T cell priming, expansion size and effector versus memory cell fates, however, it is not clear whether they can also modulate the functional features of memory CD8+ T cells. We observed that OT-I cells that were primed with weak cognate antigen signals incorporate more cytokine signals, leading to a hypothesis that CD8+ T cells that receive weak TCR signals require cytokine signals to form functional memory. Using a previously described mouse model in which IL-2 signaling via its high affinity receptor CD25 is selectively impaired, the “Il2ramut/mut” mouse, we conducted a comparative analysis of gene expression and epigenetic landscape of Il2ramut/mut and WT OT-I memory cells that were primed with strong (Lm-Ova N4) versus weak (Lm-Ova T4). RNA seq data showed that both TCR and IL-2 priming signals have minimal effect on gene expression in resting memory CD8 T cells, but they significantly modify the epigenetic landscape of the memory CD8 T cells. These findings have important contributions to the current understanding of how priming signals program memory CD8 T cells in vivo.
2020-09-30 | GSE152393 | GEO