Ontology highlight
ABSTRACT:
PROVIDER: PRJNA750800 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15312442_1.fastq.gz | Fastqsanger.gz | |||
| SRR15312442_2.fastq.gz | Fastqsanger.gz | |||
| SRR15312443_1.fastq.gz | Fastqsanger.gz | |||
| SRR15312443_2.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the impact of Influenza A virus (IAV) infection on thymic development of mouse regulatory T cells (Tregs) and conventional T cells (Tconv), the TCR repertoire of thymic Tregs and Tconv of IAV-infected and control mice was analyzed.
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Project description:Foxp3+CD4+ regulatory T cells (Tregs) play important roles in controlling both homeostatic processes and immune responses at the tissue and organismal levels. For example, Tregs promote muscle regeneration in acute or chronic injury models by direct effects on local muscle progenitor cells as well as on infiltrating inflammatory cells. Muscle Tregs have a transcriptome, a T cell receptor (TCR) repertoire and effector capabilities distinct from those of classical, lymphoid-organ Tregs, but it has proven difficult to study the provenance and functions of these unique features due to the rarity of muscle Tregs and their fragility upon isolation. Here, we attempted to side-step these hindrances by generating, characterizing and employing a line of mice carrying rearranged transgenes encoding the TCRα and TCRβ chains from a Treg clone rapidly and specifically expanded within acutely injured hindlimb muscle of young mice. Tregs displaying the transgene-encoded TCR preferentially accumulated in injured hindlimb muscle in a TCR-dependent manner both in the straight transgenic model and in adoptive-transfer systems; non-Treg CD4+ T cells expressing the same TCR did not specifically localize in injured muscle. The definitive muscle-Treg transcriptome was not established until the transgenic Tregs inhabited muscle. When crossed onto the mdx model of Duchenne muscular dystrophy, the muscle-Treg TCR transgenes drove enhanced accumulation of Tregs in hindlimb muscles and improved muscle regeneration. These findings invoke the possibility of harnessing muscle Tregs or their TCRs for treatment of skeletal muscle pathologies.
2019-12-31 | GSE140419 | GEO
Project description:Regulatory T cells (Tregs) suppress other immune cells and are indispensable for human health, yet the molecular mechanisms of suppression remain incompletely understood. Tregs can suppress proliferation and cytokine production of CD4+CD25- conventional T cells (Tcons). We previously demonstrated that human Tregs rapidly suppress T cell receptor (TCR)-induced calcium, NFAT and NF-κB pathways in Tcons, leading to inhibition of effector cytokine transcription (Schmidt A et al., Science Signaling 2011 Dec 20;4(204):ra90. doi: 10.1126/scisignal.2002179). Due to the short time period required to induce suppression, it is probable that Tregs alter protein modifications, such as (de)phosphorylations, in suppressed Tcons to cause this inhibition of particular TCR signaling events, while de novo production of repressor proteins seems unlikely. Thus, in order to identify causative factors which initiate rapid Treg-mediated suppression of Tcons, we compared phosphoproteomes of 5 minutes TCR-stimulated responder Tcons re-isolated from cocultures with primary human Tregs with those from control cocultures (Tcons cocultured with other Tcons). In addition, we measured the basal state of the phosphoproteome in unstimulated Tcon of the same donors. In total, we provide phosphoproteomics data of primary human CD4+CD25- T cells from three human healthy donors each for (i) unstimulated Tcons, (ii) 5 minutes TCR-stimulated Tcons, (iii) 5 minutes TCR-stimulated and Treg-suppressed Tcons.
2017-08-28 | PXD004291 | Pride
Project description:Recent studies have demonstrated that mature regulatory T cells ( Tregs) develop in the thymus via two pathways involving distinct Treg progenitors (TregP) - CD25+FOXP3- (CD25+ TregP) and CD25-FOXP3lo (FOXP3lo TregP) Treg progenitors. To examine this process in more detail we carried out single-cell RNA-Seq and TCR-Seq on sorted CD4+CD8+ double-positive (DP) thymocytes, CD4+ Ssingle -positive (CD4SP)P thymocytes, CD25+ TregP, FOXP3lo TregP, mature CD25+FOXP3+ Tregs and recirculating/long-term resident Tregs (RT-Tregs). Sorted populations were individually hashtagged and then combined into one scRNA-Seq/TCR-Seq library before sequencing and subsequent analysis. We found that both CD25+ TregP and FOXP3lo TregP arise via an initial agonist activated state that gives rise to a second transitional stage before differentiating into mature Tregs. Using both scRNA-Seq and bulk RNA-Seq on sorted thymocyte subsets we demonstrate that CD25+Foxp3- TregP are significantly enriched for Il2 production, suggesting that they are the major source of IL-2 needed to convert TregP into mature Tregs. Using TCR-Seq we found that several TCRs were clearly biased in favor of the conventional or Treg lineages, but that a large fraction of TCRs were found in both these lineages. Finally, we found that recirculating/resident Tregs in the thymus are not monomorphic, but are composed of multiple distinct subsets and that these RT-Tregs express the most diverse TCR repertoire of all CD4SP thymcocytes. Thus, our studies define multiple stages of Treg differentiation within the thymus, and serve as a resource for future studies on CD4+ thymocyte development and Treg differentiation.
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Project description:CD4+ regulatory T cells (Tregs) activate and expand in response to many different types of injuries, suggesting that they play a critical role in controlling the host response to tissue damage. Here we use multi-dimensional profiling techniques to comprehensively characterize injury responsive Tregs in mice. CD44high Tregs expand in response to injury and are more suppressive than CD44low Tregs. T cell receptor (TCR) analysis reveal that CD44high Tregs undergo TCRαβ clonal expansion and increased CDR3 diversity in response to injury. Bulk and single-cell RNA sequencing with paired TCR clonotype analysis demonstrate that important Treg-associated genes were significantly differentially expressed in both CD44high and CD44low Tregs with expanded TCR clonotypes. CyTOF analysis verified protein expression of these genes on CD44high Tregs, with increases in Helios, Galectin-3 and PYCARD expression following injury. Collectively, these data provide new insights into CD44high Tregs, an important subset in the response to injury to tissue damage.
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Project description:CD4+ regulatory T cells (Tregs) activate and expand in response to many different types of injuries, suggesting that they play a critical role in controlling the host response to tissue damage. Here we use multi-dimensional profiling techniques to comprehensively characterize injury responsive Tregs in mice. CD44high Tregs expand in response to injury and are more suppressive than CD44low Tregs. T cell receptor (TCR) analysis reveal that CD44high Tregs undergo TCRαβ clonal expansion and increased CDR3 diversity in response to injury. Bulk and single-cell RNA sequencing with paired TCR clonotype analysis demonstrate that important Treg-associated genes were significantly differentially expressed in both CD44high and CD44low Tregs with expanded TCR clonotypes. CyTOF analysis verified protein expression of these genes on CD44high Tregs, with increases in Helios, Galectin-3 and PYCARD expression following injury. Collectively, these data provide new insights into CD44high Tregs, an important subset in the response to injury to tissue damage.
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Project description:Temporal analysis of T-cell receptor (TCR) repertoire has been used to monitor treatment-induced changes in antigen-specific T cells in patients with cancer. However, lack of experimental model that allows the temporal analysis of TCR repertoire in same individual in homogeneous population limit the understanding of causal relationship between changes in TCR repertoire and antitumor responses. A bilateral tumor model, in which tumor cells were inoculated into the bilateral backs of mice, can be used for temporal analysis in TCR repertoire. In this study, we examined the prerequisite for this strategy: TCR repertoire are conserved between the bilateral tumor with same growth rate. The bilateral tumors with equivalent tumor size and draining lymph nodes (dLN) were collected 13 days after the tumor inoculation to analyze the TCR repertoire of CD4+ and CD8+ T cells. Most of the tumor-infiltrating T-cell clones were highly conserved between the bilateral tumors, and the extent of clonal expansion was equivalent. In addition, the similarity between bilateral tumors were equivalent to the heterogeneity in one side of the tumor. The similarity of TCR repertoire in the bilateral dLN was markedly lower than that of the tumor, suggesting that tumor-reactive T-cell clones induced independently in each dLN were integrated during recirculation and then infiltrated the tumor. These findings suggest that our bilateral tumor model is suitable for temporal monitoring of TCR repertoire to evaluate temporal and treatment-induced changes in tumor-reactive T-cell clones.
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