Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA376102 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5274670.fastq.gz | Fastqsanger.gz | |||
| SRR5274661.fastq.gz | Fastqsanger.gz | |||
| SRR5274671.fastq.gz | Fastqsanger.gz | |||
| SRR5274662.fastq.gz | Fastqsanger.gz | |||
| SRR5274672.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 13 |
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Project description:During chronic infection memory T cells acquire a unique phenotype and become dependent on different survival signals than those needed for memory T cells generated during an acute infection. The distinction between the role of effector and memory T cells in an environment of persistent antigen remains unclear. Here, in the context of chronic Toxoplasma gondii infection we demonstrate that a population of CD8 T cells exhibiting a tissue resident memory (TRM) phenotype persists in the brain. We show that this population is distributed throughout the brain in both parenchymal and extraparenchymal spaces. Furthermore, this population is transcriptionally distinct and exhibits a transcriptional signature consistent with the TRM observed in acute viral infections.
2017-06-12 | GSE95105 | GEO
Project description:Tissue-resident memory T cells (Trm) play a central role in regional immunity within non lymphoid tissues to efficiently protect against reinfection as well as to control persistent pathogen infection. Although single-cell transcriptomics analysis of Trm in various diseases have uncovered a phenotypic and functional heterogeneity of Trm, the underlying molecular mechanisms directing such diversity are poorly defined. To better understand these mechanisms, we used the model of infection with the parasite Toxoplasma gondii (T. gondii), which establishes a persistent infection in the central nervous system (CNS) controlled by brain CD8+ Trm. Through single-cell transcriptomic analysis of brain CD8+ T cells from T.gondii-infected mice, we uncovered that brain Trm subsets have an heterogenous expression of the transcriptional regulator Id2, and that these differences in Id2 levels correlated with different functional states. Using mixed bone marrow chimeras, our results revealed that T-cell specific Id2-deficiency caused parasite-specific Trm to develop an aberrant phenotype in a cell-intrinsic manner, characterized by diminished effector functions and reduced expression of the tissue retention molecules CD49a and CXCR6. This phenotype was similarly observed upon overexpression of E2A, a transcription factor negatively regulated by Id2, in parasite-specific CD8+ T cells. Conversely, the loss of Id2 in brain-infiltrating CD8+ T cells led to the accumulation of exhausted PD1+ Tox+ CD8+ Trm cells, whereas Id2 overexpression repressed the acquisition of the exhaustion phenotype and promoted the accumulation of pathogen-specific CD8+ T cells in the brain. Overall, our study indicates that Id2 expression level dictates the acquisition of an effector vs. exhausted phenotype by CD8+ Trm during chronic CNS pathogen infection.
2025-05-22 | GSE270492 | GEO
Project description:Expression profile microarray of human foreskin fibroblast cell comparing control untreated HFF cell with HFF cell infected with ME49 strain.Study on Toxoplasma gondii infection of HFF cell LncRNAs expression, for further studies on the differential exprssion of LncRNAs in HFF cell against the infection of Toxoplasma gondii research provide the basic function.
2017-01-01 | GSE92603 | GEO
Project description:Primary brain tumors, residing behind the blood-brain-barrier (BBB), have few infiltrated T cells. We hypothesized that Toxoplasma gondii, a microorganism that naturally traffics to the brain to elicit a Th1 response, can promote T cell infiltration into brain tumors. Using a mouse genetic model for medulloblastoma, we found that T. gondii infection was well-controlled in tumor-bearing mice, induced robust infiltration of T cells into the tumor, and led to myeloid cell transcriptional reprogramming toward a T cell-supportive state. The study demonstrates that the immune modulatory capacity of T. gondii could be leveraged to promote brain tumor immunotherapy through future efforts.
2024-08-22 | GSE268162 | GEO
Project description:The outcome of infections with Toxoplasma gondii in humans is dependent in part on the genetic makeup of the infecting organism. Recent studies have indicated that most infecting Toxoplasma organisms fall into 1 of 3 canonical lineages. Previous studies have investigated the effects of Toxoplasma on its host cell transcriptome. Little is known, however, about the effects of three canonical lineages on brain cells, the principal site of parasite lifelong persistence. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to T. gondii infection using microarray analysis to characterize the strain-specific host cell response to 3 canonical T. gondii strains. We found that the extent of the expression changes varied considerably among the three strains. Neuroepithelial cells infected with type I exhibited the most differential gene expression, whereas type II infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to central nervous system while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter expression of a clearly defined set of genes. Moreover, Ingenuity pathway analysis (IPA) revealed the sophistication of different strain in its interactions with the host. These differences may explain some of the variation in the neurobiological effects of different strains of Toxoplasma on infected individuals. We infected SK-N-MC cells with 3 canonical Toxoplasma strains and assessed their gene expression in RNA at 20 hours post-infection using Affymetrix GeneChip. Infections and controls (no tachyzoites) were performed in duplicate and experiments for each strain were carried out on three separate occasions in order to include both technical replicates and biological replicates.
2011-06-24 | E-GEOD-22986 | biostudies-arrayexpress
Project description:MicroRNA expression of mouse brain induced by Toxoplasma gondii oocysts
| PRJNA418218 | ENA
Project description:The outcome of infections with Toxoplasma gondii in humans is dependent in part on the genetic makeup of the infecting organism. Recent studies have indicated that most infecting Toxoplasma organisms fall into 1 of 3 canonical lineages. Previous studies have investigated the effects of Toxoplasma on its host cell transcriptome. Little is known, however, about the effects of three canonical lineages on brain cells, the principal site of parasite lifelong persistence. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to T. gondii infection using microarray analysis to characterize the strain-specific host cell response to 3 canonical T. gondii strains. We found that the extent of the expression changes varied considerably among the three strains. Neuroepithelial cells infected with type I exhibited the most differential gene expression, whereas type II infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to central nervous system while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter expression of a clearly defined set of genes. Moreover, Ingenuity pathway analysis (IPA) revealed the sophistication of different strain in its interactions with the host. These differences may explain some of the variation in the neurobiological effects of different strains of Toxoplasma on infected individuals.
2011-06-24 | GSE22986 | GEO
Project description:Small intestine intraepithelial CD4+ T cells after Toxoplasma gondii infection
| PRJNA238368 | ENA
Project description:Toxoplasma gondii is a ubiquitous protozoan pathogen able to infect both mammalian and avian hosts. Surprisingly, just three strains appear to account for the majority of isolates from Europe and N. America. To test the hypothesis that strain divergence might be driven by differences between mammalian and avian response to infection, we examine in vitro strain-dependent host responses in a representative avian host, the chicken. Chicken embryonic fibroblasts were cultivated in vitro and infected with different strains of Toxoplasma gondii; host transcriptional responses were then analyzed at 24 hours post-infection.
2011-05-27 | E-GEOD-29563 | biostudies-arrayexpress
Project description:The protozoan pathogen Toxoplasma gondii has the unique ability to develop a chronic infection in the brain of its host. The T. gondii develops cysts within the neurons that are resilient against the host immune response and current therapeutics. The bradyzoite parasites within the cyst have a sugar-protein-rich wall and a slow-replication cycle, allowing them to remain hidden from the host. This intracellular encysted lifestyle of T. gondii has made them recalcitrant to molecular analysis in vivo. Here, we have enriched for T. gondii brain cysts 21 to 150 days post-infection (DPI). RNA and protein from bradyzoites was isolated from each timepoint. Deep sequencing of transcripts expressed during these three timepoints showed many of the identified proteins are transcriptionally expressed at a high level. Approximately one-third are more enriched during bradyzoite conditions compared to tachyzoites, and approximately half are expressed at similar levels during each phase. We have expanded the transcriptional profile of in vivo bradyzoites to 120 DPI. The RNA sequencing depth of in vivo bradyzoite T. gondii was over 250-fold greater than was have been previously, which allowed us to identify low level transcripts and novel bradyzoite-specific isoforms.
2019-07-11 | GSE134099 | GEO