TCR repertoire profiling of T cells expressing NK-cell markers
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq 2000
ORGANISM(S): Homo sapiens
SUBMITTER: Ivan Zvyagin
PROVIDER: E-MTAB-9601 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The presented data corresponds to the analysis of two discrete subsets of human CD8+ naive T cells, defined by positive and negative expression of the chemokine receptor CXCR3 (TNR3-, TNR3+). In this study we demonstrated that these subsets have different potential to generate fully-differentiated effector T cells following antigen-specific stimulation. The performed systematic immune repertoire analysis (T cell receptor beta chain (TRB)) of the sorted cell subsets revealed diverse physico-chemical properties of TRB CDR3 sequences suggesting enhanced TCR self-reactivity in human TNR3+ cells. In total, we analyzed 74 samples (from 11 patients, 3 replicates of each cell subset (excluding one missing replicate) and additionally for 3 patients CD8+ memory T cells in 3 replicates). We used the Human TCR Profiling Kit (MiLaboratory LLC) for sequencing libraries preparation and Illumina NextSeq 550 sequencing (150+150bp) followed by the demultiplexing procedure using MIGEC software (https://github.com/mikessh/migec).
2019-10-17 | E-MTAB-7638 | biostudies-arrayexpress
Project description:In this work, we studied clonal T-cell repertoires of synovial fluid from a large cohort of SpA patients aiming to characterise the TCR repertoire structure and to identify specific T-cell clonal expansions
2023-05-31 | E-MTAB-11498 | biostudies-arrayexpress
Project description:To track for T cell clones from donor memory T cell fraction infused after abT/CD19-depleted allogenic HSCT we performed TCR beta repertoire sequencing. Patient peripheral blood repertoire was sequenced in two timepoints (p3 and p4: d120-180 and d360-500). Reperotoires for bulk and CD4+ or CD8+ cells from CD45RA-depleted donor apheresis were obtained for most donor-recipient pairs. TCR beta cDNA libraries were prepared using previously published protocol (Zvyagin I.V. et al., Leukemia, 2017). Libraries were sequenced on Illumina NextSeq 500/550 and HiSeq2000/2500 in pair-end mode with read length 100-150 bp. MiGEC software were used for demultiplexing and unique molecular identifier sequence extraction software (https://github.com/mikessh/migec).
2020-07-01 | E-MTAB-8874 | biostudies-arrayexpress
Project description:To investigate novel molecular signatures and transcriptional regulators of immature and mature human NK cells, we performed whole-genome microarray analysis on dNK cells (CD3−CD56+), cNK cells (CD3−CD56+), pNK cells (CD3−CD56+), CD56+ T cells (CD3+CD56+) and T cells (CD3+CD56−). dNK cells were purified from first-trimester deciduas. cNK cells were purified from cord-blood mononuclear cells. pNK, CD56+ T and T cells were purified from adult peripheral blood mononuclear cells. Samples were collected from healthy adult donors after obtaining informed consent according to the Ethics Committee of the University of Science & Technology of China.
2013-02-10 | GSE24268 | GEO
Project description:TCR repertoire profiling of T cells expressing NK-cell markers
| PRJEB40492 | ENA
Project description:A small subset of T cells also expresses kiler-cell immunoglobulin-like receptors (KIRs). We find that KIR+ T cells primarily reside in the CD56+ T population. However, little is known on how these cells are different from the conventional CD56- T, NK, and iNKT cells. We used microarray profiling to compare and determine the distinctive differences of CD56+ T cell and its KIR subsets when compared to the conventional CD56- T, NK and iNKT cells. Lymphocyte subsets were sorted from human peripheral blood mononuclear cells with FACSAriaII (BD Biosciences, San Jose, CA) using anti-CD3, anti-CD56, anti-CD14, anti-KIR2DL1, anti-KIR2DL2/3, anti-KIR3DL1 and anti-TCRValpha24 antibodies. The purity of CD3+CD56- T cells, CD3-CD56+ NK cells, CD3+CD56+ T cells, KIR-CD3+CD56+ T cells, and KIR+CD3+CD56+ T cells were more than 98% in all experiments. The purities of iNKT cells for TCRValpha24 and CD1d-tetramer were >95% and >90%, respectively. RNA pre-amplification, labeling and hybridization on Human Genome U133Plus 2.0 GeneChip array were performed in the St. Jude Hartwell Center for Bioinformatics & Biotechnology microarray core facility according to the manufacturer’s instructions (Affymetrix, Santa Clara, CA).
2013-07-01 | E-GEOD-47855 | biostudies-arrayexpress
Project description:To define the physiological properties of TCR signaling, We investigated the global dynamic view of TCR-dependent phosphorylation with the use of thymocytes stimulated with antibodies to CD3 to mimic TCR activation
2022-02-22 | PXD000969 | Pride
Project description:We sorted Eomes-negative NK cells (CD3- CD56+ CXCR6- CD16-) and Eomes-positive NK cells (CD3- CD56+ CXCR6+) from total leukocytes isolated from the perfusion fluid of five healthy human livers destined for transplantation. Total RNA was extracted from sorted cells, cDNA generated and RNASeq performed.
2016-09-28 | GSE87392 | GEO
Project description:Our previous work demonstrated that HIV-1 infection progressively reduces TCR/CD3 expression due to a defect in CD3g gene transcripts. We further found that knocking down expression of the viral tat and/or nef genes was correlated with CD3g transcript and TCR/CD3 surface receptor levels on HIV-1 infected cells. This study was undertaken to investigate the direct effect of HIV-1 Tat expression on the TCR/CD3 machinery. Progressive downregulation from TCR/CD3hi to TCR/CD3lo to TCR/CD3? was observed on Tat expressing cells in a manner that emulated HIV-1 infection, with a lack of CD3g transcripts again responsible for the defect. When Tat cell cultures containing a mixture of TCR/CD3 surface densities were separated into TCR/CD3hi and TCR/CD3lo/? populations, they quickly reverted to a mixed CD3 phenotype. Thus, the progression TCR/CD3hi to TCR/CD3lo to TCR/CD3? is an active, reversible process with receptor levels fluctuating in response to intracellular dynamics. Examination of tat mutants found that the regions involved in Tat-mediated transactivation and TAR binding are required for TCR/CD3 downregulation while the lysine at position 28 and Tat exon 2 are dispensable. Global gene expression, assessed in association with TCR/CD3 downregulation in HIV-1 infected and Tat expressing cells, detected broad suppression of TCR/CD3 signaling, co-stimulation and negative regulatory genes along with target transcription factors, ligands and receptors. A significant subset of the genes altered in HIV-1 infected cells was specifically targeted by Tat in association with TCR/CD3 loss. Our finding that Tat negatively regulates many facets of the TCR/CD3 machinery has important implications for disease pathogenesis. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-12-31 | E-GEOD-32626 | biostudies-arrayexpress
Project description:Our previous work demonstrated that HIV-1 infection progressively reduces TCR/CD3 expression due to a defect in CD3g gene transcripts. We further found that knocking down expression of the viral tat and/or nef genes was correlated with CD3g transcript and TCR/CD3 surface receptor levels on HIV-1 infected cells. This study was undertaken to investigate the direct effect of HIV-1 Tat expression on the TCR/CD3 machinery. Progressive downregulation from TCR/CD3hi to TCR/CD3lo to TCR/CD3â was observed on Tat expressing cells in a manner that emulated HIV-1 infection, with a lack of CD3g transcripts again responsible for the defect. When Tat cell cultures containing a mixture of TCR/CD3 surface densities were separated into TCR/CD3hi and TCR/CD3lo/â populations, they quickly reverted to a mixed CD3 phenotype. Thus, the progression TCR/CD3hi to TCR/CD3lo to TCR/CD3â is an active, reversible process with receptor levels fluctuating in response to intracellular dynamics. Examination of tat mutants found that the regions involved in Tat-mediated transactivation and TAR binding are required for TCR/CD3 downregulation while the lysine at position 28 and Tat exon 2 are dispensable. Global gene expression, assessed in association with TCR/CD3 downregulation in HIV-1 infected and Tat expressing cells, detected broad suppression of TCR/CD3 signaling, co-stimulation and negative regulatory genes along with target transcription factors, ligands and receptors. A significant subset of the genes altered in HIV-1 infected cells was specifically targeted by Tat in association with TCR/CD3 loss. Our finding that Tat negatively regulates many facets of the TCR/CD3 machinery has important implications for disease pathogenesis. We used microarrays to investigate changes in CD4+ T cell gene expression induced by HIV-1 infection for comparison with the Tat expressing cells. Examine changes in gene expression in TCR/CD3 negative HIV-1 infected cells compared to TCR/CD3 positive uninfected controls.
2015-12-31 | E-GEOD-33706 | biostudies-arrayexpress