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Functional heterogeneity of human memory T cell clones primed by pathogens or vaccines

ABSTRACT: It is unclear to what extent T helper cells with a different phenotype (chemokine receptor and cytokine production profile) are generated in response to pathogen challenge or vaccination, and whether such heterogeneity can arise among the progeny of a single precursor. We combined cellular methods to isolate antigen specific T cells from different T helper memory subsets of human donors, and next generation sequencing of their TCR. This approach revealed a high level of heterogeneity in the phenotype of human T cells responding to different pathogens/vaccines also at a clonal level, as we could characterize cells bearing an identical T cell receptor with divergent effector properties.

ORGANISM(S): Homo sapiens

PROVIDER: GSE64852 | GEO | 2015/01/13

SECONDARY ACCESSION(S): PRJNA272412

REPOSITORIES: GEO

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Functional heterogeneity of human memory T cell clones primed by pathogens or vaccines

Project description:It is unclear to what extent T helper cells with a different phenotype (chemokine receptor and cytokine production profile) are generated in response to pathogen challenge or vaccination, and whether such heterogeneity can arise among the progeny of a single precursor. We combined cellular methods to isolate antigen specific T cells from different T helper memory subsets of human donors, and next generation sequencing of their TCR. This approach revealed a high level of heterogeneity in the phenotype of human T cells responding to different pathogens/vaccines also at a clonal level, as we could characterize cells bearing an identical T cell receptor with divergent effector properties. NGS-based analysis of T cell receptor repertoire of T helper memory cells identical gross specificity (i.e. responding to a given pathogen or vaccine antigen) belonging to different heper subsets (Th1, Th2, Th17)

2015-01-13 | E-GEOD-64852 | biostudies-arrayexpress

Multi-omic analysis reveals dynamic changes of three-dimensional chromatin architecture during T cell differentiation (Hi-C)

Project description:Background: Activation of T cells results in widespread changes in transcriptional programs and multi-level remodeling of three-dimensional genome architecture. Although many efforts have been made in dissecting the epigenomic regulation during T cell activation and differentiation, it remains to be investigated in depth how alterations in the local and global chromatin structure coordinate gene expression in this process. Results: We characterize dynamic changes at different levels of chromatin organization during Naive CD4+ T (Naive) differentiation into T helper 17 (Th17) and T helper 1 (Th1) cells using Hi-C, RNA-Seq and ATAC-Seq assays. As a result of T cell activation, extensive changes occur at the transcriptome, chromatin accessibility and higher-order structure levels. We observe decreased short-range chromatin interactions and increased extra-long-range chromatin interactions upon activation. At compartment level, although A/B compartments have no apparent global switch, the intensity of compartmentalization markedly alters in activated T cells. At TAD level, a fraction of TADs is rearranged with increase TAD number upon activation. In addition, we identify promoter-enhancer (P-E) loops, many of which are associated with T cell activation or cell-type specificity, including Rorc encoding RORγt (retinoic-acid-receptor-related orphan receptor gamma t) that facilitates Th17 differentiation and Hif1a (hypoxia-inducible factor 1α) that responds to intracellular oxygen levels in Th1. Conclusion: T cell activation is conserved at multiple levels across T helper cells and species. From the 3D genome perspective, these results provide fresh insights into heterogeneity and plasticity of T helper cells during T cell activation based on chromatin reorganization.

2023-07-03 | GSE210418 | GEO

Multi-omic analysis reveals dynamic changes of three-dimensional chromatin architecture during T cell differentiation (ATAC-Seq)

2023-07-03 | GSE210417 | GEO

Multi-omic analysis reveals dynamic changes of three-dimensional chromatin architecture during T cell differentiation (RNA-Seq)

2023-07-03 | GSE210416 | GEO

The CD4+ alike CD8+ memory T cell compartment diversification reveales CD8+ T cell subsets with cytotoxic and non-cytotoxic properties

Project description:CD4+ memory T helper cells are organized in different subsets characterized by distinct functions and chemokine receptor expression patterns induced and maintained by divergent gene programs. We demonstrate here that identical chemokine receptor combinations are sufficient to separate analogous differentiated CD8+ memory T cell subsets with matching cytokine profiles. Tc2, Tc17 and Tc22 type CD8+ T cell subsets, in contrast to classical cytotoxic Tc1 and Tc17+1 cells, possess a CD4 helper type alike phenotype characterized by absent cytotoxicity and SLAMF7 expression as well their ability to express CD40L upon activation. Their highly disparate homing patterns and unique TCR repertoire associates them to distinct immune responses as compared to those cytotoxic CD8+ T cells exert their role in. The dermal T cell gene expression signature and enrichment in psoriasis patients indicates that peripheral helper type CD8+ T cells represent a circulatory variant of skin resident cells.

2020-08-25 | GSE115103 | GEO

Chimpanzee adenoviral vectors as vaccines for outbreak pathogens.

Project description: Not available

| S-EPMC5718829 | biostudies-other

Cancer stem cells subpopulations within the CD44high human breast cancer stem cell compartment [HMT clones]

Project description:The CD44hi compartment in human breast cancer is enriched in tumor-initiating cells, however the functional heterogeneity within this subpopulation remains poorly defined. From a human breast cancer cell line with a known bi-lineage phenotype we have isolated and cloned CD44hi populations that exhibited mesenchymal/Basal B and luminal/Basal A features, respectively:CD44+/CD24-,Basal B (G4, H6) cells and CD44hi/CD24lo epithelioid Basal A (A4, AB) cells. Seven replicates of A4, seven replicates of G4, three replicates of AB, three replicates of H6

2015-04-30 | E-GEOD-59281 | biostudies-arrayexpress

Cancer stem cells subpopulations within the CD44high human breast cancer stem cell compartment [HMT clones]

2015-04-30 | GSE59281 | GEO

CD4+ cell transcriptional profiling by RNA sequencing

Project description:<p>We use next generation sequencing to investigate the different transcriptomes of closely related CD4+ T-cells from healthy human donors to elucidate the genetic programs that underlie their specialized immune functions. Six cell types were included: Regulatory T-cells (CD25hiCD127low/neg with >95% FOXP3+ purity), regulatory T-cells activated using PMA/ionomycin, CD25-CD45RA+ ('naive' helper T-cells), CD25-CD45RO+ ('memory' helper T-cells), activated Th17 cells (>98% IL17A+ purity) and activated IL17-CD4+ T-cells (called 'ThPI'). Poly-T capture beads were used to isolate mRNA from total RNA, and fragment sizes of ~200 were sequenced from both ends on Illumina's genome analyzer. We confirm many of the canonical signature genes of T-cell populations, but also discover new genes whose expression is limited to specific CD4 T-cell lineages, including long non-coding RNAs. Additionally, we find that genes encoded at loci linked to multiple human autoimmune diseases are enriched for preferential expression upon T-cell activation, suggesting that an aberrant response to T-cell activation is fundamental to pathogenesis.</p>

| phs000626 | dbGaP

Selvaggio2020 - Microenvironment control of hybrid Epithelial-Mesenchymal phenotypes

Project description:Epithelial to Mesenchymal Transition (EMT) has been associated with cancer cell heterogeneity, plasticity and metastasis. It has been the subject of several modeling effort. This logical model of the EMT cellular network aims to assess microenvironmental signals controlling cancer-associated phenotypes amid the EMT continuum. Its outcomes relate to the qualitative degrees of cell adhesions by adherent junctions and focal adhesions, two features affected during EMT. Model attractors recover epithelial, mesenchymal and hybrid phenotypes, and simulations show that hybrid phenotypes may arise through independent molecular paths, involving stringent extrinsic signals. Of particular interest, model predictions and their experimental validations indicated that: 1) ECM stiffening is a prerequisite for cells overactivating FAK-SRC to upregulate SNAIL1 and acquire a mesenchymal phenotype, and 2) FAK-SRC inhibition of cell-cell contacts through the Receptor Protein Tyrosine Phosphates kappa leads to the acquisition of a full mesenchymal rather than a hybrid phenotype.

2020-06-30 | MODEL2004040001 | BioModels

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