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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 Our unpublished observations indicate that mice lacking the CD8+ T cell cytolytic effector molecule, Granzyme B, (GzmB), are resistant to ECM, showing markedly reduced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.

ORGANISM(S): Mus musculus

PROVIDER: GSE24903 | GEO | 2010/12/10

SECONDARY ACCESSION(S): PRJNA132091

REPOSITORIES: GEO

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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 Our unpublished observations indicate that mice lacking the CD8+ T cell cytolytic effector molecule, Granzyme B, (GzmB), are resistant to ECM, showing markedly reduced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. 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.

2010-12-10 | E-GEOD-24903 | biostudies-arrayexpress

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

Gene expression analysis of GzmB-/- hematopoietic stem cells (HSC).

Project description:This study aimed to compare the expression profile of GzmB deficient HSCs and their WT counterparts in order to understand their phenotype in bone marrow in vivo reconstitution assays. GzmB-/- HSC mRNA expression was compared to WT counterparts. Samples of 3 biological replicates (pool of 3 mice per replicate) of each group has been used for the array.

2014-04-11 | E-GEOD-56574 | biostudies-arrayexpress

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

2007-10-11 | GSE6019 | 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

Gene expression analysis of GzmB-/- hematopoietic stem cells (HSC).

2014-04-11 | GSE56574 | GEO

Regulatory B cells expressing granzyme B (GZMB+Bregs)

Project description:Regulatory B cells expressing granzyme B (GZMB+Bregs)

| PRJNA931282 | ENA

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

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

Long Non-coding RNA LINC02474 Affects Metastasis and Apoptosis of Colorectal Cancer by Inhibiting the Expression of GZMB

Project description:Background: Colorectal cancer (CRC) is one of the most frequently diagnosed malignancies. Metastasis is the main event that impedes the therapeutic effect on CRC, and its underlying mechanisms remain largely unclear. LINC02474 is a novel long noncoding RNA (lncRNA) associated with metastasis of CRC, while little is known about how LINC02474 regulates these malignant characteristics. Methods: Expressions of LINC02474 and granzyme B (GZMB) were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blotting analysis. Cell metastasis was detected by transwell assay and metastatic nude mouse model, and apoptosis was determined by Western blotting analysis and ﬂow cytometry. Besides, the interaction between LINC02474 and GZMB was detected by dual-luciferase reporter assays. Results: The expression of LINC02474 was signiﬁcantly up-regulated in CRC tissues. Moreover, depletion of LINC02474 damaged the metastatic abilities of CRC cells in vivo and in vitro while boosting apoptosis. Besides, up-regulation of LINC02474 could promote migration and invasion, while apoptosis was inhibited in CRC cells. Besides, down-regulation of LINC02474 promoted the expression of GZMB, and interference of GZMB could increase the metastatic abilities of CRC cells while reducing apoptosis. Furthermore, LINC02474 was related to the transcriptional repression of GZMB in CRC cells determined by the dual-luciferase reporter assay. Conclusions: The ﬁndings revealed that a novel lncRNA, LINC02474, as an oncogene, could promote metastasis, but limit apoptosis partly by impeding GZMB expression in CRC. Besides, LINC02474 had the potential to be used as a biomarker in the prognosis of CRC.

2021-03-27 | GSE169722 | GEO

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