Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA771240 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16351803.fastq.gz | Fastqsanger.gz | |||
| SRR16351804.fastq.gz | Fastqsanger.gz | |||
| SRR16351805.fastq.gz | Fastqsanger.gz | |||
| SRR16351806.fastq.gz | Fastqsanger.gz | |||
| SRR16351807.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
Similar Datasets
Project description:T cells bearing gamma delta T cell antigen receptors (TCRs) function in lymphoid stress surveillance. However, the contribution of gamma delta TCRs to such responses is unclear. Here we found that the TCR of a human V gamma4Vdelta5 clone directly bound endothelial protein C receptor (EPCR), which allowed gamma delta T cells to recognize both endothelial cells targeted by cytomegalovirus and epithelial tumors. EPCR is a major histocompatibility complex–like molecule that binds lipids analogously to the antigen-presenting molecule CD1d. However, the V gamma4Vdelta5 TCR bound EPCR independently of lipids, in an antibody-like way. Moreover, the recognition of target cells by gamma delta T cells required a multimolecular stress signature composed of EPCR and costimulatory ligand(s). Our results demonstrate how a gamma delta TCR mediates recognition of broadly stressed human cells by engaging a stress-regulated self antigen. 2E9 is an antibody that blocks gd-TCR recognition of human cells that are the targets of the clone LES. 2E9 also stains cells that are targeted by LES. Therefore, to identify the TCR ligand expressed by 2E9-positive cells, Gene Expression was compared in two cell lines that stain with 2E9 (K562 and U937) versus two cell lines that do not (Hutu80 and Huh7).
2012-07-27 | E-GEOD-39709 | biostudies-arrayexpress
Project description:Identification of Ligands for the human gamma-delta TCR
| PRJNA171513 | ENA
Project description:T cells bearing gamma delta T cell antigen receptors (TCRs) function in lymphoid stress surveillance. However, the contribution of gamma delta TCRs to such responses is unclear. Here we found that the TCR of a human V gamma4Vdelta5 clone directly bound endothelial protein C receptor (EPCR), which allowed gamma delta T cells to recognize both endothelial cells targeted by cytomegalovirus and epithelial tumors. EPCR is a major histocompatibility complex–like molecule that binds lipids analogously to the antigen-presenting molecule CD1d. However, the V gamma4Vdelta5 TCR bound EPCR independently of lipids, in an antibody-like way. Moreover, the recognition of target cells by gamma delta T cells required a multimolecular stress signature composed of EPCR and costimulatory ligand(s). Our results demonstrate how a gamma delta TCR mediates recognition of broadly stressed human cells by engaging a stress-regulated self antigen.
2012-07-28 | GSE39709 | GEO
Project description:HLA-DR-lacking HSPCs [HLA-DR(-) HSPCs] were detected in aplastic anemia (AA) patients with HLA-DR15. HLA-DR(-) HSPCs may evade the attack by CD4+ T-cells recognizing the autoantigen presented by HLA-DR15. The goal of this study is to clarify the immune escape mechanisms from antigen-specific T-cells by comparing the trranscriptome profile of HLA-DR(+) HSPCs and HLA-DR(-) HSPCs.
2022-05-31 | GSE183768 | GEO
Project description:The contribution of chronic antigen stimulation to the occurrence of lymphoproliferative disorder (LPD) with the gamma-delta T-cell lineage is unclear, despite the fact that Epstein-Barr virus (EBV) positive T-cell LPD is derived from antigen-stimulated cytotoxic T-cells. Given the possible association of antigen stimulation with the development of cytotoxic T-cell LPD, we compared gene expression patterns in Epstein-Barr virus (EBV)-positive gamma-delta T-cell lines derived from patients with nasal T-cell lymphoma and chronic active EBV infection and those in gamma-delta T-cells from healthy volunteers. Three EBV-positive gamma-delta T-cells lines, SNT cells (SNT-8, SNT-13 and SNT-15), were used in this study. SNT-8 was established from patients with nasal T-cell lymphoma and SNT-13, -15 were established from patients with chronic active EBV infection (Zhang Y, et al., Br J Cancer 94:599-608, 2006). All the SNT cells exhibits common rearrangement of Vgamma9-JgammaP and Jdelta3 genes. The gamma-delta T-cells obtained from healthy volunteers were expanded ex vivo by 1 microM of zoledronate (ZOL) plus IL-2 for 14 days incubation. Experiment Overall Design: We compared gene expression profiling in 3 EBV-positive positive gamma-delta T-cells lines with those in gamma-delta T cells obtaied from a healthy volunteer. Global gene expression was analyzed using the Affymetrix Human Genome U133 2.0 Plus GeneChip Set. Analysis of variance (ANOVA) was done using GeneSifter® (VizXLabs). Values of P<0.05 were considered to be a statistically significant difference.
2009-12-18 | E-GEOD-13906 | biostudies-arrayexpress
Project description:T-cell Acute Lymphoblastic Leukemia (T-ALL) is a lymphoid malignancy characterized by clonal proliferation of immature thymocytes arrested at particular stage of differentiation. Earlier studies from our lab have demonstrated that 30% of Indian T-ALL patients exhibited clonal rearrangement of both TCR γ and δ genes. The survival was higher in T-ALL patients showing clonal rearrangements for TCR γ and δ genes. In the present study, we aimed at investigating the gene expression profiles of TCR γδ+ T-ALL patients and correlating it with functional analysis to understand the reasons for increased survival in these patients. Our studies demonstrate differential expression of genes in TCR γδ clonal T-ALL compared to non TCR γδ clonal T-ALL patients. Functional annotation of significantly upregulated genes (p<0.05) in TCR γδ+ T-ALL patients showed involvement in antigen processing and presentation, cell-cell communication, apoptosis, cell adhesion molecules and immune synapse pathways. Expression of eight selected genes (SMAD3, NFkB1, HLA-DQB1, SOCS2, CISH, FASLG, RXRA,and IFNβ1) was validated in TCRαβ+ and TCRγδ+ subgroups of T-ALL patients using quantitative Real-time PCR. Studies focusing on functional aspects of the gene(s) identified from gene expression profile would aid in developing future therapeutic strategies.
2016-04-25 | GSE37389 | GEO
Project description:The contribution of chronic antigen stimulation to the occurrence of lymphoproliferative disorder (LPD) with the gamma-delta T-cell lineage is unclear, despite the fact that Epstein-Barr virus (EBV) positive T-cell LPD is derived from antigen-stimulated cytotoxic T-cells. Given the possible association of antigen stimulation with the development of cytotoxic T-cell LPD, we compared gene expression patterns in Epstein-Barr virus (EBV)-positive gamma-delta T-cell lines derived from patients with nasal T-cell lymphoma and chronic active EBV infection and those in gamma-delta T-cells from healthy volunteers. Three EBV-positive gamma-delta T-cells lines, SNT cells (SNT-8, SNT-13 and SNT-15), were used in this study. SNT-8 was established from patients with nasal T-cell lymphoma and SNT-13, -15 were established from patients with chronic active EBV infection (Zhang Y, et al., Br J Cancer 94:599-608, 2006). All the SNT cells exhibits common rearrangement of Vgamma9-JgammaP and Jdelta3 genes. The gamma-delta T-cells obtained from healthy volunteers were expanded ex vivo by 1 microM of zoledronate (ZOL) plus IL-2 for 14 days incubation.
2009-12-09 | GSE13906 | GEO
Project description:Microarray expression data from human TCRVg9-positive gamma delta T lymphocytes
| PRJNA137339 | ENA
Project description:Gamma-delta T cells are potent anti-cancer effectors with the potential to target tumours broadly, independent of patient-specific neoantigens or HLA background. Gamma-delta T cells can sense conserved cell stress signals prevalent in transformed cells, although the mechanisms behind the targeting of stressed target cells remain poorly characterized. Vg9Vd2 T cells – the most abundant subset of human gamma-delta T cells – recognize a protein complex containing butyrophilin 2A1 (BTN2A1) and BTN3A1, a widely expressed cell surface protein that is activated by phosphoantigens abundantly produced by tumour cells. Here, we layered genome-wide CRISPR screens in target cancer cells to identify pathways that regulate: (1) killing by gamma-delta T cells during co-culture, and (2) BTN3A cell surface expression. In addition to confirming the importance of the phosphoantigen-producing mevalonate pathway, the screens revealed previously unappreciated multilayered regulation of BTN3A abundance on the cell surface and triggering of gamma-delta T cells through transcription, post-translational modifications, membrane trafficking. Notably, IRF1 and ZNF217 were discovered to be positive and negative transcriptional regulators that directly occupy the promoters of BTN3A1/2/3 genes. In addition, diverse genetic perturbations and inhibitors disrupting metabolic pathways in the cancer cells, particularly ATP-producing processes, were found to alter BTN3A levels. This induction of BTN3A, as well as BTN2A1, during metabolic crises was dependent on AMP-activated protein kinase (AMPK). Finally, small molecule activation of AMPK in a cell line model and in patient-derived tumour organoids led to increased expression of the BTN2A1-BTN3A complex and increased Vg9Vd2 TCR-mediated killing. This AMPK-dependent mechanism of metabolic stress-induced ligand upregulation deepens our understanding of gamma-delta T cell stress surveillance and suggests new avenues to enhance gamma-delta T cell anti-cancer activity.
2023-05-05 | GSE192828 | GEO
Project description:Gamma-delta T cells are potent anti-cancer effectors with the potential to target tumours broadly, independent of patient-specific neoantigens or HLA background. Gamma-delta T cells can sense conserved cell stress signals prevalent in transformed cells, although the mechanisms behind the targeting of stressed target cells remain poorly characterized. Vg9Vd2 T cells – the most abundant subset of human gamma-delta T cells – recognize a protein complex containing butyrophilin 2A1 (BTN2A1) and BTN3A1, a widely expressed cell surface protein that is activated by phosphoantigens abundantly produced by tumour cells. Here, we layered genome-wide CRISPR screens in target cancer cells to identify pathways that regulate: (1) killing by gamma-delta T cells during co-culture, and (2) BTN3A cell surface expression. In addition to confirming the importance of the phosphoantigen-producing mevalonate pathway, the screens revealed previously unappreciated multilayered regulation of BTN3A abundance on the cell surface and triggering of gamma-delta T cells through transcription, post-translational modifications, membrane trafficking. Notably, IRF1 and ZNF217 were discovered to be positive and negative transcriptional regulators that directly occupy the promoters of BTN3A1/2/3 genes. In addition, diverse genetic perturbations and inhibitors disrupting metabolic pathways in the cancer cells, particularly ATP-producing processes, were found to alter BTN3A levels. This induction of BTN3A, as well as BTN2A1, during metabolic crises was dependent on AMP-activated protein kinase (AMPK). Finally, small molecule activation of AMPK in a cell line model and in patient-derived tumour organoids led to increased expression of the BTN2A1-BTN3A complex and increased Vg9Vd2 TCR-mediated killing. This AMPK-dependent mechanism of metabolic stress-induced ligand upregulation deepens our understanding of gamma-delta T cell stress surveillance and suggests new avenues to enhance gamma-delta T cell anti-cancer activity.
2023-05-04 | GSE226931 | GEO