Highly cross-reactive and competent effectors dominate the CD8+ T cell response in Trypanosoma cruzi infection
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1091607 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR28440229_1.fastq.gz | Fastqsanger.gz | |||
| SRR28440229_2.fastq.gz | Fastqsanger.gz | |||
| SRR28440231_1.fastq.gz | Fastqsanger.gz | |||
| SRR28440231_2.fastq.gz | Fastqsanger.gz |
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Project description:CD8+ T cells are key effectors in immune control of Trypanosoma cruzi infection. Within C57BL/6 mice, the T. cruzi-specific CD8+ T cell response is higly focused on several immunodominant epitopes including TSKb20. These immunodominant epitopes all elicit non-protective T cell responses that are entirely dispensable for immune control, suggesting that other, subdominant CD8+ T cells of unknown specificities might play an important role in mediating parasite control. We assessed the relative effector capacity of TSKb20 T cells compared to other responding T cells at the site of reinfection using paired scRNA and TCR sequencing to evaluate the gene expression profiles of particular T cell clonotypes.
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Project description:As Trypanosoma cruzi, the etiological agent of Chagas disease, multiplies in the cytoplasm of nucleated host cells, infection with this parasite is highly likely to affect host cells. We performed an exhaustive transcriptome analysis of T. cruzi-infected HeLa cells using an oligonucleotide microarray containing probes for greater than 47,000 human gene transcripts. In comparison with uninfected cells, those infected with T. cruzi showed greater than threefold up-regulation of 41 genes and greater than threefold down-regulation of 23 genes. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of selected, differentially expressed genes confirmed the microarray data. Many of these up- and down-regulated genes were related to cellular proliferation, including seven up-regulated genes encoding proliferation inhibitors and three down-regulated genes encoding proliferation promoters, strongly suggesting that T. cruzi infection inhibits host cell proliferation, which may allow more time for T. cruzi to replicate and produce its intracellular nests. These findings provide new insight into the molecular mechanisms by which intracellular T. cruzi infection influences the host cell, leading to pathogenicity. Keywords: infection response
2008-02-06 | GSE7047 | GEO
Project description:To generate a high quality, annotated gene expression database of T. cruzi trypomastigotes(TRP), amastigotes (AMA), epimastigotes (EPI), and metacyclic trypomastigotes (MET). The global assessment of transcript abundances in each life-cycle stage of T. cruzi will identify stage-regulated genes and provide an essential element of an integrated database of T. cruzi genomic, proteomic, and transcriptomic data. RNAs from 3 biological replicates from a single time point in each stage will be subjected to DNA microarrays containing probes for the complete, annotated T. cruzi genome, as it is currently known. The arrays for this project will be provided by the Pathogen Functional Genomics Resource Center (PFGRC) at The Institute for Genomic Research (TIGR) sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), and will contain long oligonucleotides complementary to every annotated gene in the newly sequenced T. cruzi genome. The resulting data and analysis results will be deposited in TcruziDB (http://TcruziDB.org). Keywords: Gene expression comparisons between the four life-cycle stages of T. cruzi
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Project description:Trypanosoma cruzi is a protozoan parasite and the etiologic agent of Chagas disease, an important public health problem in Latin America. T. cruzi is diploid, almost exclusively asexual, and displays an extraordinarily diverse population structure both genetically and phenotypically. Yet, to date the genotypic diversity of T. cruzi and its relationship, if any, to biological diversity have not been studied at the whole genome level. In this study, we used whole genome oligonucleotide tiling arrays to compare gene content in biologically disparate T. cruzi strains by comparative genomic hybridization (CGH). We observed that T. cruzi strains display widespread and focal copy number variations (CNV) and a substantially greater level of diversity than can be adequately defined by the current genetic typing methods. As expected, CNV were particularly frequent in gene family-rich regions containing mucins and trans-sialidases but were also evident in core genes. Gene groups that showed little variation in copy numbers among the strains tested included those encoding protein kinases and ribosomal proteins, suggesting these loci were less permissive to CNV. Moreover, frequent variation in chromosome copy numbers were observed, and chromosome-specific CNV signatures were shared by genetically divergent T. cruzi strains, suggesting a greater degree of chromosome exchange than previously thought.
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Project description:Antibody recognition of Trypanosoma cruzi conserved proteins was assessed by evaluating pools of patient IgG samples on microarrays of 400,000 peptides covering these proteins as 15-mers with an overlap of 13 amino acids.
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Project description:Host cell infection by the intracellular pathogen, Trypanosoma cruzi, involves activation of signaling pathways, cytoskeletal reorganization, and targeted recruitment of host cell lysosomes. To determine the consequences of T. cruzi invasion on host cell gene expression, high density microarrays consisting of ~27,000 human cDNAs were hybridized with fluorescent probes generated from T. cruzi-infected human fibroblasts (HFF) at early time points following infection (2-24 h). Surprisingly, no genes were induced 2-fold in HFF between 2 and 6 h post-infection (hpi) in repeated experiments while immediate repression of six host cell transcripts was observed. A significant increase in transcript abundance for 106 host cell genes was observed at 24 hpi. Among the most highly induced is a set of interferon-stimulated genes, indicative of a type I interferon (IFN) response to T. cruzi. In support of this, T. cruzi-infected fibroblasts begin to secrete IFN at 18 hpi following the induction of IFN transcripts. As compared with global transcriptional responses evoked by other intracellular pathogens, T. cruzi is a stealth parasite that elicits few changes in host cell transcription during the initiation of infection.
2005-09-26 | E-SMDB-1560 | biostudies-arrayexpress
Project description:Host cell infection by the intracellular pathogen, Trypanosoma cruzi, involves activation of signaling pathways, cytoskeletal reorganization, and targeted recruitment of host cell lysosomes. To determine the consequences of T. cruzi invasion on host cell gene expression, high density microarrays consisting of approximately 27,000 human cDNAs were hybridized with fluorescent probes generated from T. cruzi-infected human fibroblasts (HFF) at early time points following infection (2-24 h). Surprisingly, no genes were induced > or =2-fold in HFF between 2 and 6 h post-infection (hpi) in repeated experiments while immediate repression of six host cell transcripts was observed. A significant increase in transcript abundance for 106 host cell genes was observed at 24 hpi. Among the most highly induced is a set of interferon-stimulated genes, indicative of a type I interferon (IFN) response to T. cruzi. In support of this, T. cruzi-infected fibroblasts begin to secrete IFNbeta at 18 hpi following the induction of IFNbeta transcripts. As compared with global transcriptional responses evoked by other intracellular pathogens, T. cruzi is a stealth parasite that elicits few changes in host cell transcription during the initiation of infection.
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