Resident T Cell Repertoires
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA802671 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17848400_1.fastq.gz | Fastqsanger.gz | |||
| SRR17848400_2.fastq.gz | Fastqsanger.gz | |||
| SRR17848401_1.fastq.gz | Fastqsanger.gz | |||
| SRR17848401_2.fastq.gz | Fastqsanger.gz | |||
| SRR17848402_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 50 |
Similar Datasets
Project description:Regulatory T (Treg) are present in lymphoid and non-lymphoid tissues and restrict immune activation, prevent autoimmunity and regulate inflammation. While Treg in non-lymphoid tissues are typically resident, Treg in lymph nodes (LNs) predominantly recirculate and residency of Treg in LNs is poorly studied. Here, we show that 10-20% of all Treg in LNs are memory-like resident cells. Both thymic and peripheral Treg contributed to the pool of resident Treg and their residency did not require continuous TCR signaling. Yet, resident and circulating Treg had distinct TCR repertoires and different LNs contained distinct clonal subpopulations of resident Treg. We speculate that stochastic selection and variation in antigen availability governs commitment of individual T cell clones to the resident pool in each LN. Our results describe a framework for local fine-tuning of immune responses in LNs based on previous adaptive immune responses.
2022-02-04 | GSE195930 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE32348: Methylation specifies distinct estrogen-induced binding site repertoires of CBP to chromatin (mRNA) GSE32349: Methylation specifies distinct estrogen-induced binding site repertoires of CBP to chromatin (ChIP-Seq) Refer to individual Series
2011-10-06 | E-GEOD-32350 | biostudies-arrayexpress
Project description:Deep sequencing of recombined T cell receptor (TCR) genes and transcripts has provided a view of T cell repertoire diversity at an unprecedented resolution. Beyond profiling peripheral blood, analysis of tissue-resident T cells provides further insight into immune-related diseases. We describe the extraction of TCR sequence information directly from RNA-sequencing data from 6738 tumor and 604 control tissues, with a typical yield of 1 TCR per 10 million reads. This method circumvents the need for PCR amplification of the TCR template and provides TCR information in the context of global gene expression, allowing integrated analysis of extensive RNA-sequencing data resources.
| S-EPMC4666197 | biostudies-literature
Project description:Developing B lymphocytes undergo V(D)J recombination to assemble germline V, D, and J gene segments into exons that encode the antigen-binding variable region of immunoglobulin (Ig) heavy (H) and light (L) chains. IgH and IgL chains associate to form the B cell receptor (BCR), which upon antigen binding activates B cells to secrete BCR as an antibody. Each of the huge number of clonally independent B cells expresses a unique set of IgH and IgL variable regions. Ability of V(D)J recombination to generate vast primary B cell repertoires results from combinatorial assortment of large numbers of different V, D, and J segments, coupled with diversification of the junctions between them to generate the complementary determining region 3 (CDR3) for antigen contact. Approaches to evaluate in depth the content of primary antibody repertoires and, ultimately, to study how they are further molded by secondary mutation and affinity maturation processes are of great importance to the B cell development, vaccine, and antibody fields. We now describe an unbiased, sensitive, and readily accessible assay, referred to as HTGTS repertoire sequencing (HTGTS-Rep-seq), to quantify antibody repertoires. HTGTS-Rep-seq quantitatively identifies the vast majority of IgH and IgL V(D)J exons, including their unique CDR3 sequences, from progenitor and mature mouse B lineage cells via the use of specific J primers. HTGTS-Rep-seq also accurately quantifies DJH intermediates and V(D)J exons in either productive or non-productive configurations. HTGTS-Rep-seq should be useful for studies of human samples, including clonal B-cell expansions and also for following antibody affinity maturation processes. We employed high-throughput genome-wide translocation sequencing adapted repertoire sequencing (HTGTS-Rep-seq) to study antibody repertoires. For HTGTS-Rep-seq libraries, we utilize bait coding ends of J segments to identify, in unbiased fashion, mouse IgH DJH repertoires [processed tlx files] along with both productive and non-productive IgH V(D)J repertoires from both pro-B and peripheral B cells [processed xls files of samples 1-18, 21-51]. Similarly, we also identify mouse productive and non-productive Igk repertoires from peripheral B cells [processed xls files of samples 19,20,52-57].
2016-07-22 | E-GEOD-82126 | biostudies-arrayexpress
Project description:Early B cell development is orchestrated by the combined activities of the transcriptional regulators E2A, EBF1, Foxo1 and Ikaros. However, how the genome-wide binding patterns of these regulators are modulated during B-lineage development remains to be determined. Here, we found that in lymphoid progenitors the chromatin remodeler Brg1 specified the B cell fate. In committed pro-B cells Brg1 regulated Igh locus contraction and controlled c-Myc expression to modulate the expression of genes that regulate ribosome biogenesis. In committed pro-B cells Brg1 also suppressed a pre-B lineage-specific pattern of gene expression. Finally, we found that Brg1 acted mechanistically to establish B cell fate and modulate cell growth by facilitating access of lineage-specific transcription factors to poised enhancer repertoires. 8 ATAC-Seq samples from sorted ALP and BLP (duplicates, control and Brg1-deleted), 4 ATAC-Seq samples from cultured pro-B cells (duplicates, control and Brg1-deleted), 2 Ikaros ChIP-seq samples (performed in Rag1-/- pro-B cells and in E2A-/- pre-pro-B cells), 1 Brg1 ChIP-seq sample and accompanying Input sample (both in Rag1-/- pro-B cells), 4 RNA-Seq samples from cultured pro-B cells (duplicates, control and Brg1-deleted), 6 RNA-Seq samples from cultured Rag1-/- pro-B cells (triplicates, control and Brg1-knock down).
2015-05-15 | E-GEOD-66978 | biostudies-arrayexpress
Project description:Early B cell development is orchestrated by the combined activities of the transcriptional regulators E2A, EBF1, Foxo1 and Ikaros. However, how the genome-wide binding patterns of these regulators are modulated during B-lineage development remains to be determined. Here, we found that in lymphoid progenitors the chromatin remodeler Brg1 specified the B cell fate. In committed pro-B cells Brg1 regulated Igh locus contraction and controlled c-Myc expression to modulate the expression of genes that regulate ribosome biogenesis. In committed pro-B cells Brg1 also suppressed a pre-B lineage-specific pattern of gene expression. Finally, we found that Brg1 acted mechanistically to establish B cell fate and modulate cell growth by facilitating access of lineage-specific transcription factors to poised enhancer repertoires.
2015-05-15 | GSE66978 | GEO
Project description:Recent studies have documented genome-wide binding patterns of transcriptional regulators and their associated epigenetic marks in hematopoietic cell lineages. In order to determine how epigenetic marks are established and maintained during developmental progression, we have generated long-term cultures of hematopoietic progenitors by enforcing the expression of the E-protein antagonist Id2. Hematopoietic progenitors that express Id2 are multipotent and readily differentiate upon withdrawal of Id2 expression into committed B lineage cells, thus indicating a causative role for E2A in promoting the B cell fate. Genome-wide analyses revealed that a substantial fraction of lymphoid and myeloid enhancers are pre-marked by H3K4me1 in multipotent progenitors. However, H3K4me1 levels at a subset of enhancers are elevated during developmental progression, resulting in evolving enhancer repertoires that we propose orchestrate the myeloid and B cell fates. ChIP-Seq and gene expression profiling were performed in an inducible hematopoietic pluripotent cell line that can be differentiated into multiple lymphoid lineages. This submission contains ChIP-Seq data. Recent studies have demonstrated a tight correlation between transcriptionally active promoters and H3K4 trimethylation, whereas H3K4 monomethylation has been associated with enhancer activity. To determine whether the changes in gene expression patterns upon differentiation correlate with the presence of H3K4me3 as well as H3K4me1, ChIP-sequencing was performed on these two marks on cell lysates that were derived from Id2-HPCs and differentiated Id2-HPCs. The H3K4me1 marks were further analyzed to investigate the dynamics of enhancer repertoires between these cells. Id2-HPCs were cultured in IMDM medium supplemented with 10% FCS/2% PSG/M-NM-2-me and IL7, Flt3-ligand, and SCF cytokines on S17 feeder cells in a humidified incubator at 37 degrees C with 5% CO2. Id2-HPC expanded cells were depleted of small (<1-5%) numbers of CD19-, CD25- and CD11b-positive cells by auto-MACS. For myeloid differentiation, cells were cultured for up to 6 days in IMDM medium supplemented with 10% FCS/2% PSG/M-NM-2-me and IL3, Flt3L, GMCSF and MCSF cytokines. To promote B-cell differentiation, cells were cultured for up to 5 days in IMDM medium supplemented with 10% FCS/2% PSG/M-NM-2-me and IL-7 and SCF cytokines on S17 feeder cells in the presence of 1 ug/mL doxycycline, or alternatively, in alpha-MEM medium in the presence of cytokines and on Tst-4 stromal cells.
2011-09-01 | E-GEOD-30858 | biostudies-arrayexpress
Project description:Regulatory T cells (Treg) are present in lymphoid and non-lymphoid tissues where they restrict immune activation, prevent autoimmunity and regulate inflammation. Treg in non-lymphoid tissues are typically resident, while those in lymph nodes (LNs) are considered to recirculate. However, Treg in LNs are not a homogenous population and circulation kinetics of different Treg subsets are poorly characterized. Furthermore, whether Treg can acquire memory T cell properties and persist for extended periods after their activation in LNs is unclear. Here, we used in situ labeling with a stabilized photoconvertible protein to uncover turnover rates of Treg in LNs in vivo. We found that while the majority of Treg in LNs recirculate, 10-20% are memory-like resident cells that remain in their respective LNs for weeks to months. Single cell RNA sequencing revealed that LN-resident cells are a functionally and ontogenetically heterogeneous population and share the same core residency gene signature with conventional CD4+ and CD8+ T cells. Resident cells in LNs did not actively proliferate and did not require continuous TCR signaling for their residency. Yet, resident and circulating Treg had distinct TCR repertoires, and each LN contained exclusive clonal subpopulations of resident Treg. Our results demonstrate that, similar to conventional T cells, Treg can form resident memory-like populations in LNs after adaptive immune responses. Specific and local suppression of immune responses by resident Treg in draining LNs might provide new therapeutic opportunities for the treatment of local chronic inflammatory conditions.
2023-08-23 | GSE235702 | GEO
Project description:Antibody repertoires in peanut allergy
| PRJNA378451 | ENA