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Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment [Treg patients]

ABSTRACT: Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment [Treg patients]

PROVIDER: PRJNA733055 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14664427_1.fastq.gz	Fastqsanger.gz
	SRR14664427_2.fastq.gz	Fastqsanger.gz
	SRR14664428_1.fastq.gz	Fastqsanger.gz
	SRR14664428_2.fastq.gz	Fastqsanger.gz
	SRR14664429_1.fastq.gz	Fastqsanger.gz

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Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment [Treg patients]

Project description:Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment [Treg patients]

| PRJNA733055 | ENA

Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment

Project description:Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment

| PRJNA733049 | ENA

Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment [Treg_HD]

Project description:Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment [Treg_HD]

| PRJNA733053 | ENA

Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment [Treg patients]

Project description:Human FOXP3+ regulatory T (Treg) cells are central to immune tolerance. However, their heterogeneity and differentiation remain incompletely understood. Here we use single-cell RNA and T cell receptor sequencing to resolve Treg cells from healthy individuals and patients with or without acute graft-versus-host disease (aGVHD) who undergo stem cell transplantation. These analyses, combined with functional assays, separate Treg cells into naïve/activated/effector stages, and resolve the HLA-DRhi, LIMS1hi, highly suppressive FOXP3hi, and highly proliferative MKI67hi effector subsets. Trajectory analysis assembles Treg subsets into two differentiation paths (I/II) with distinctive phenotypic/functional programs, ending with the FOXP3hi and MKI67hi subsets, respectively. Transcription factors FOXP3 and SUB1 contribute to some Path I and Path II phenotypes, respectively. These FOXP3hi and MKI67hi subsets and two differentiation pathways are conserved in transplanted patients, despite having functional/migratory impairments under aGVHD. The findings expand the understanding of Treg cell heterogeneity and differentiation and provide a single-cell atlas for the dissection of Treg complexity in health and disease.

2021-05-27 | GSE175603 | GEO

Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment [Treg_HD]

2021-05-27 | GSE175602 | GEO

Single-cell Transcriptomic Analysis Reveals Disparate Effector Differentiation Pathways in Human Treg Compartment

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-27 | GSE175604 | GEO

Treg cells from human blood differentiate into non-lymphoid tissue-resident effector cells upon TNFR2 costimulation

Project description:Regulatory T (Treg) cells can facilitate transplant tolerance and attenuate autoimmune- and inflammatory diseases. Therefore, it is clinically relevant to stimulate Treg cell expansion and function in vivo and to create therapeutic Treg cell products in vitro. We report that TNF receptor 2 (TNFR2) is a unique costimulus for naïve, thymus-derived (t)Treg cells from human blood that promotes their differentiation into non-lymphoid tissue (NLT)-resident effector Treg cells, without Th-like polarization. In contrast, CD28 costimulation maintains a lymphoid tissue (LT)-resident Treg cell phenotype. We base this conclusion on transcriptome and proteome analysis of TNFR2- and CD28-costimulated CD4+ Treg cells and conventional T (Tconv) cells, followed by bioinformatic comparison with published transcriptomic Treg cell signatures from NLT and LT in health and disease, including autoimmunity and cancer. These analyses illuminate that TNFR2 costimulation promotes Treg cell capacity for survival, migration, immunosuppression and tissue regeneration. Functional studies confirmed improved migratory ability of TNFR2-costimulated tTreg cells. Flow cytometry validated the presence of the TNFR2-driven Treg cell signature in effector/memory Treg cells from the human placenta as opposed to blood. Thus, TNFR2 can be exploited as driver of NLT-resident Treg cell differentiation for adoptive cell therapy or antibody-based immunomodulation in human disease.

2024-01-24 | PXD048248 | Pride

Sequence analysis of CD4 Treg, CD8 Treg and CD8 effector

Project description:Sequence analysis of CD4 Treg, CD8 Treg and CD8 effector

| PRJNA633028 | ENA

Sequence analysis of CD4 Treg, CD8 Treg and CD8 effector

Project description:We show that Ly49+CD122+ CD8+ Treg have a distinct expression profie compared to conventional Foxp3+ CD4+ Treg and CD49 lo CD122+ CD8 effector like cells. RNA was extracted from sorted cells and sent for sequencing

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Bach2 represses effector programmes to stabilize Treg-mediated immune homeostasis

Project description:Through their functional diversification, CD4+ T cells play key roles in both driving and constraining immune-mediated pathology. Transcription factors are critical in the generation and maintenance of cellular diversity and negative regulators antagonistic to alternate fates often act in conjunction with positive regulators to stabilize lineage specification1. Polymorphisms within the locus encoding a transcription factor BACH2 are associated with diverse immune-mediated diseases including asthma2, multiple sclerosis3, Crohn¹s disease4-5, coeliac disease6, vitiligo7 and type 1 diabetes8. A role for Bach2 in maintaining immune homeostasis, however, has not been established. Here, we define Bach2 as a broad regulator of immune activation that stabilizes immunoregulatory capacity while repressing the differentiation programmes of multiple effector lineages in CD4+ T cells. Bach2 was required for efficient formation of regulatory (Treg) cells and consequently for suppression of lethal inflammation in a manner that was Treg cell dependent. Assessment of the genome-wide function of Bach2, however, revealed that it represses genes associated with effector cell differentiation. Consequently, its absence during Treg polarization resulted in inappropriate diversion to effector lineages. In addition, Bach2 constrained full effector differentiation within Th1, Th2 and Th17 cell lineages. These findings identify Bach2 as a key regulator of CD4+ T-cell differentiation that prevents inflammatory disease by controlling the balance between tolerance and immunity. The role of Bach2t to regulate immune homeostasis was investigated by mapping DNA binding profiles of Bach2 in iTreg condition. The function of Bach2 was also evaluated by comparing transcriptome in WT and Bach2-deficient iTreg cells and further comparison was done with transcriptome in naive, Th1, Th2, and Th17 conditions.

2013-06-27 | E-GEOD-45975 | biostudies-arrayexpress

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