Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Splenic CD4 T cells in naïve C57BL/6 mice or during Plasmodium berghei ANKA infection in C57BL/6 and B6.GzmB-/- mice.

ABSTRACT: Infection of C57BL/6 mice with Plasmodium berghei ANKA (PbA) is a well-established experimental model of cerebral malaria (ECM). ECM is characterised by high levels of parasite sequestration and recruitment of pathogenic CD8+ T cells to the brain. The role of CD4+ T cells in this model has not yet been fully elucidated, although our laboratory has recently shown that CD4+ T cell depletion prior to infection results in significantly lower parasite burdens and protection from ECM. These data highlight a pathogenic role for CD4+ T cells in ECM. Our unpublished observations indicate that mice lacking the CD8+ T cell cytolytic effector molecule, Granzyme B, (GzmB), are resistant to ECM, showing markedly reduced parasite burdens. Late depletion of CD4+ T cells from PbA-infected GzmB-deficient mice results in enhanced parasite burdens, indicating that these cells may play an anti-parasitic role. In the present study, we have analysed splenic CD4+ T cell gene expression profiles in naïve C57BL/6 mice, and PbA-infected wild-type and GzmB-deficent mice to further our understanding of the CD4+ T cell response in ECM. Splenic CD4 T cells isolated by cell sorting from either uninfected C57BL/6 or PbA-infected C57BL/6 or B6.GzmB-/- mice at day 4 post-infection. Total RNA obtained from four mice per group.

ORGANISM(S): Mus musculus

SUBMITTER: Ashraful Haque

PROVIDER: E-GEOD-24903 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Splenic CD4 T cells in naïve C57BL/6 mice or during Plasmodium berghei ANKA infection in C57BL/6 and B6.GzmB-/- mice.

Project description:Infection of C57BL/6 mice with Plasmodium berghei ANKA (PbA) is a well-established experimental model of cerebral malaria (ECM). ECM is characterised by high levels of parasite sequestration and recruitment of pathogenic CD8+ T cells to the brain. The role of CD4+ T cells in this model has not yet been fully elucidated, although our laboratory has recently shown that CD4+ T cell depletion prior to infection results in significantly lower parasite burdens and protection from ECM. These data highlight a pathogenic role for CD4+ T cells in ECM. Our unpublished observations indicate that mice lacking the CD8+ T cell cytolytic effector molecule, Granzyme B, (GzmB), are resistant to ECM, showing markedly reduced parasite burdens. Late depletion of CD4+ T cells from PbA-infected GzmB-deficient mice results in enhanced parasite burdens, indicating that these cells may play an anti-parasitic role. In the present study, we have analysed splenic CD4+ T cell gene expression profiles in naïve C57BL/6 mice, and PbA-infected wild-type and GzmB-deficent mice to further our understanding of the CD4+ T cell response in ECM.

2010-12-10 | GSE24903 | GEO

Transcription profiling of mouse blood from native and Plasmodium berghei induced experimental cerebral malaria untreated or treated with activated charcoal.

Project description:We found that oral activated charcoal (oAC) provided significant protection against P. berghei ANKA-induced ECM, significantly increasing overall survival time compared to untreated mice. Protection from ECM by oAC was associated with a reduced numbers of splenic TNF+ CD4+ T cells and multifunctional IFNy+TNF+ CD4+ and CD8+ T cells. Furthermore, we identified a whole blood gene expression signature (68 genes) associated with protection from ECM. To evaluate whether oAC might affect current best available anti-malarial treatment, a group of female C57BL/6 mice infected with PbA received Activated Charcoal. At day 6 p.i., and prior to the first deaths of untreated PbA-infected mice, 5 untreated PbA-infected mice (Group 1) and 5 AC-treated PbA-infected mice (Group 2) were killed and fresh blood (300-500�l per mouse) was collected and processed into RNA. Blood was also taken from uninfected control mice (�baseline�- Group 3).

2010-04-01 | E-MEXP-2594 | biostudies-arrayexpress

Cerebral malaria is regulated by host mediated changes in Plasmodium gene expression

Project description:Cerebral Malaria (CM), the deadliest complication of Plasmodium infection, is a complex and unpredictable disease. Currently, our understanding of the factors that trigger progression of malaria to CM is limited. Here, by infecting experimental CM (ECM) resistant (Balb/c) and ECM susceptible (C57BL/6) mice with ECM causing (ANKA) and non-ECM causing (NK65) Plasmodium berghei (Pb) parasite strains, we revealed that in resistant host, infection by ECM causing parasite develops similar to infection by non-ECM causing parasite in susceptible host in terms of parasite growth in host, disease course and host immune response against parasite. Our comparative gene expression analysis revealed that in Balb/c host, gene expression of Pb ANKA parasite is remarkably different from, the gene expression of Pb ANKA in C57BL/6 but similar to the gene expression of non-ECM causing Pb NK65 in C57BL/6. Thus, host has a critical influence on parasite behavior which ultimately determines the course of malaria disease.

2023-02-21 | GSE215359 | GEO

MHC II immunopeptidome during Plasmodium berghei blood stage infection

Project description:In malaria, T cells play a dual role by both restricting parasite growth and mediating immunopathology such as the deadly neuroinflammation called cerebral malaria. During experimental cerebral malaria (ECM), IFN produced by CD4 T cells promotes CD8 T cell sequestration in brain capillaries, resulting in endothelial damage, oedema and death. However the antigen-presenting cells controlling the development of CD4 T cell responses, as well as the antigens recognized by these CD4 T cells, are unknown. Here we used mass spectrometry to characterize the MHC II immunopeptidome presented by dendritic cells during blood stage malaria in C57BL/6 mice. We identified 14 MHC II ligands derived from 13 conserved Plasmodium berghei proteins that we validated in vivo. This work profiles the first MHC II immunopeptidome in a mouse model of blood stage malaria.

2017-09-20 | PXD007628 | Pride

Transcriptional Reprogramming of Mature CD4 T helper Cells generates distinct MHC class II restricted Cytotoxic T Lymphocytes

Project description:We show here that the T helper-fate is not fixed and that mature antigen-stimulated CD4 T cells can switch off Thpok expression and reactivate CD8- lineage genes. This unexpected plasticity results in the post-thymic termination of the T helper- program and the functional differentiation of distinct MHC class II restricted CD4 cytotoxic T lymphocytes Small intestine CD4 intraepithelial T lymphocytes from ThPOK-GFP reposter mice were isolated and sorted (FACS Aria) based on ThPOK and CD8aa expression. Cell were isolated either from non-experimental ThPOK-GFP reporter mice (WT) or after transfering CD4 naive T cells from ThPOK-GFP reporter mice to RAG-/-recipient animals (TR) as an experimental colitis model. Experimet was done in duplicate.

2012-12-10 | E-GEOD-42277 | biostudies-arrayexpress

The critical and diverse roles of CD4-CD8- double negative T cells in non-alcoholic fatty liver disease

Project description:Methods: RNA transcription profiling of intrahepatic CD4-CD8- double negative T cells were compared between C57BL/6 mice fed with control diet and methionine-choline deficient diet (MCD) for 5 weeks. Results: RNA sequencing data showed that intrahepatic DNT in NAFLD mice exhibited markedly decreased Prf1, Gzmb but increased Il17a expression.

2021-07-22 | GSE180576 | GEO

Expression data from malaria-specific mouse CD4 T cell (PbT-II) subset after Plasmodium berghei ANKA infection

Project description:The multiple species of Plasmodium that infect humans are highly polymorphic and induce various infections ranging from asymptomatic state to severe life-threatening diseases such as cerebral malaria. However, how the differences between the parasites affect host immune responses during blood-stage infection remains largely unknown. In this study, we investigated the CD4+ T-cell immune responses in T-cell receptor-transgenic mice infected simultaneously with P. berghei ANKA (PbA) and P. chabaudi chabaudi AS (Pcc) using PbT-II cells, which recognize a common epitope of these parasites. In the acute phase of infection, CD4+ T-cell responses in PbA-infected mice showed a higher involvement of Th1 cells and a lower proportion of Ly6Clo effector CD4+ T cells than those in Pcc-infected mice. Transcriptome analysis of PbT-II cells indicated that type I interferon (IFN)-regulated genes were expressed at higher levels in both Th1- and Tfh-type PbT-II cells from PbA-infected mice than those from Pcc-infected mice. Moreover, IFN-α levels were considerably higher in PbA-infected mice than in Pcc-infected mice. Inhibition of type I IFN signaling increased PbT-II and Ly6Clo cell numbers and partially reversed the Th1 over Tfh bias of the PbT-II cells in both PbA- and Pcc-infected mice. However, in the memory phase, we did not find a significant difference in the phenotype of PbT-II cells between PbA- and Pcc-primed mice. These observations suggested that the differences in Plasmodium-specific CD4+ T-cell responses between PbA- and Pcc-infected mice were at least partially associated with the difference in type I cytokine production during the early phase of the infection.

2021-07-11 | GSE179860 | GEO

Distinct pathways of pathogenesis in mice with experimental cerebral malaria following P. berghei ANKA infection.

2007-10-11 | GSE6019 | GEO

Transcriptomic profiles of liver tissue from hindlimb unloaded mice treated with 4-phenylbutyrate

Project description:Bulk transcriptomic profiles of liver tissues from male, 18 weeks old c57Bl/6j mice, including ground-based controls, hindlimb-unloaded mice treated with vehicle, and hindlimb unloaded mice treated wit 4-phenylbutyrate (4-PBA)

2024-02-11 | GSE196560 | GEO

Transcription profiling of mouse with experimental cerebral malaria following P. berghei ANKA infection.

Project description:Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection, predominantly experienced by children and non-immune adults, which results in great mortality and long-term sequelae. Recent reports based on histology of post-mortem brain tissue suggest that CM may be the common end point for a range of syndromes. Here, we have analysed the gene expression profiles in brain tissue taken from experimental CM (ECM)-susceptible, Plasmodium berghei ANKA (PbA)-infected C57BL/6 (B6) and CBA/CaH (CBA) mice with ECM. Gene expression profiles were largely heterogeneous between the two ECM-susceptible strains. These results, combined with experimental data, support the existence of distinct pathogenic pathways in CM. Experiment Overall Design: C57BL/6 and CBA/CaH mice were infected with 10e5 Plasmodium berghei ANKA-infected RBCs and monitored for ECM development. At onset of ECM symptoms, infected mice and naive controls were culled, perfused (in order to remove non-adherent circulating cells), and brains were removed. Total RNA was extracted from these brains and pooled (n=6 mice/ group). Pooled RNA samples were converted to cDNA and antisense cRNA, labelled and hybridized to GeneChip Mouse Genome 430 2.0 Arrays (Affymetrix, Surrey Hills, Australia). Arrays were scanned using the GeneChip Scanner 3000 (Affymetrix) and GeneChip Operating Software v1.1.1 (Affymetrix). Normalisation and initial analyses were carried out in GeneSpring v7 (Agilent Technologies). Values below 0.01 were set to 0.01. Each measurement was divided by the 50th percentile of all measurements in that sample. The data was filtered for genes flagged as present, which had at least an expression level of 50. Following this, a threshold of 2.5 fold up-regulation or down-regulation of genes differentially expressed during ECM was set.

2008-06-14 | E-GEOD-6019 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data