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Gene expression in MHCII restricted mature thymocytes from Thpok-RKF- or Thpok-RKF+ Thpokfl/flRunx3fl/dYFPCd4-Cre+ mixed Bone marrow chimera.

ABSTRACT: Gene expression in MHCII restricted mature thymocytes from Thpok-RKF- or Thpok-RKF+ Thpokfl/flRunx3fl/dYFPCd4-Cre+ mixed Bone marrow chimera.

PROVIDER: PRJNA768268 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16175768_1.fastq.gz	Fastqsanger.gz
	SRR16175768_2.fastq.gz	Fastqsanger.gz
	SRR16175769_1.fastq.gz	Fastqsanger.gz
	SRR16175769_2.fastq.gz	Fastqsanger.gz
	SRR16175770_1.fastq.gz	Fastqsanger.gz

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Gene expression in MHCII restricted mature thymocytes from Thpok-RKF- or Thpok-RKF+ Thpokfl/flRunx3fl/dYFPCd4-Cre+ mixed Bone marrow chimera.

Project description:Thpok-RKF which harbors a mutation in the BTB domain and disrupts the interaction between NuRD complex could not repress CD8 and CD8 lineage genes expression in Thpokfl/flRunx3fl/dYFPCd4-Cre+ from B2m-/- host. However, Thpok-RKF upregulates CD4 expression in these mice.

2022-06-10 | GSE185217 | GEO

TCR-mediated ThPOK induction promotes development of mature (CD24-) gammadelta thymocytes.

Project description:T lymphocytes develop into two major lineages characterized by expression of the alphabeta and gammadelta T cell receptor (TCR) heterodimers. Within each major lineage, further specialization occurs, resulting in distinct subsets that differ in TCR specificity, phenotype and functional attributes. Thus, in the murine thymus, two distinct subsets of mature (CD24-) gammadelta cells have been identified, that is NK1.1+ cells, which are enriched for Vgamma1.1 usage and selectively produce IFNgamma on stimulation, and CCR6+ cells, which are enriched for Vgamma2 usage produce IL17. The upstream signals and transcriptional pathways that promote development of these distinct gammadelta subsets remain relatively poorly understood. Here, we show that the Zn-finger transcription factor ThPOK has a critical function in the development of gammadelta thymocytes. Thus, lack of functional ThPOK causes a marked reduction in the percentage and absolute number of mature gammadelta thymocytes, and a particularly severe reduction of NK1.1+ cells. Conversely, constitutive ThPOK expression leads to a striking increase in mature NK1.1+ gammadelta thymocytes. Further, we show that ThPOK induction in gammadelta thymocytes is induced by strong TCR signals mediated by engagement with antibody or high-affinity endogenous ligands, and that an important ThPOK cis-acting element, the distal regulatory element (DRE), is sufficient for this TCR-dependent induction. These results show that ThPOK expression in gammadelta thymocytes is regulated in part by the strength of TCR signalling, identify ThPOK as an important mediator of gammadelta T cell development/maturation, and lend strong support to the view that development of a significant fraction of gammadelta T cells depends on TCR engagement/signalling.

| S-EPMC2910264 | biostudies-literature

Gene Expression in Effector T cells, wildtype of Thpok-deficient

Project description:The transcription factor Thpok is essential for CD4 T cell development in the thymus and remains expressed in post-thymic CD4 T cells. We post-thymically inactivated Thpok and compared microarray gene expression in Thpok-deficient CD4 T cells to that in their wildtype CD4 or CD8 counterparts We show that Thpok constrains the transcriptional circuitry to maintain CD4+-lineage integrity in naM-CM-/ve cells and to couple effector differentiation to environmental cues after antigenic stimulation. Redundantly with the related factor LRF, Thpok is continuously needed to prevent the trans-differentiation of mature CD4+ into -CD8+ T cells. We activated naM-CM-/ve CD4 T cells (either wild-type or Thpok-deficient) and CD8 T cells (wild-type) in vitro under Th1 conditions. Differentiated effectors were sorted 4 days after activation into CD4+CD8- and CD4-CD8+ (wild-type) and CD4+CD8- and CD4+CD8+ (Thpok-deficient) subsets. Total RNA was extracted from sorted subsets and processed for microarray analyses (Affymetrix Mouse Exon 1.0 ST array) at the NCI microarray facility, following the manufacturerM-bM-^@M-^Ys recommendation. Data is from 3 replicates (except wild-type CD4-CD8+ cells, for which two samples only were processed), generated from two distinct cell preparations.

2014-08-15 | E-GEOD-57846 | biostudies-arrayexpress

Satb1 Orchestrates the Expression of Lineage-Specifying Genes in Post-Selection Thymocytes

Project description:T-cell receptor (TCR) signaling by MHC class-I and -II induces thymocytes to acquire cytotoxic and helper fates via induction of Runx3 or ThPOK transcription factors, respectively. The mechanisms by which TCR signaling is translated into transcriptional programs for each cell fate remain elusive. We show that a genome organizer, Satb1, activates genes for lineage-specifying factors, including ThPOK and Runx3, in post-selection thymocytes. Indeed, Satb1-deficient thymocytes are partially redirected to inappropriate T lineages after MHC selection. Although Satb1 is dispensable for maintaining ThPOK in CD4+ T cells, it is necessary for restraining expression of the Treg factor FoxP3. Collectively, our findings demonstrate that Satb1 shapes the primary T-cell pool by initially directing lineage-specific transcriptional programs and subsequently balancing effector versus regulatory subsets via FoxP3 repression.

2017-01-19 | GSE77000 | GEO

Transcriptional Reprogramming of Mature CD4 T helper Cells generates distinct MHC class II restricted Cytotoxic T Lymphocytes

Project description:We show here that the T helper-fate is not fixed and that mature antigen-stimulated CD4 T cells can switch off Thpok expression and reactivate CD8- lineage genes. This unexpected plasticity results in the post-thymic termination of the T helper- program and the functional differentiation of distinct MHC class II restricted CD4 cytotoxic T lymphocytes Small intestine CD4 intraepithelial T lymphocytes from ThPOK-GFP reposter mice were isolated and sorted (FACS Aria) based on ThPOK and CD8aa expression. Cell were isolated either from non-experimental ThPOK-GFP reporter mice (WT) or after transfering CD4 naive T cells from ThPOK-GFP reporter mice to RAG-/-recipient animals (TR) as an experimental colitis model. Experimet was done in duplicate.

2012-12-10 | E-GEOD-42277 | biostudies-arrayexpress

Genome-wide maps of SATB1 bound regions in thymocytes and peripheral CD4+ T lymphocytes.

Project description:T-cell receptor (TCR) signaling by MHC class-I and -II induces thymocytes to acquire cytotoxic and helper fates via induction of Runx3 or and ThPOK transcription factors, respectively. The mechanisms by The mechanisms by which TCR signaling is translated into transcriptional programs for each cell fate remain elusive. It remains elusivewhich how TCR signaling is translated into transcriptional programs for each cell fate remain elusive. We show that a genome organizer, SATB1, activates genes for lineage-specifying factors, including ThPOK, Runx3, CD4, CD8 and Treg factor Foxp3, and Treg factor Foxp3, and CD4, and /CD8, in post-selection thymocytes. Indeed, SATBatb1-deficient thymocytes are partially redirected into inappropriate T lineages after both MHC class-I and -II mediated selection, and fail to generate Treg subset. Despite its essential role in initiating regulatory regions activity in TCR signaled thymocytes. SATBatb1 is becomes dispensable for maintaining ThPOK in CD4+ T cells. Collectively, our findings demonstrate that SATBatb1 shapes the primary T-cell pool by initially directing lineage-specific transcriptional programs in the thymus.

2017-05-23 | GSE90635 | GEO

Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function [RNA-seq]

Project description:The transcription factor ThPOK is critical for homeostasis and differentiation of mature T helper cells. Overall goal of this experiment is to show divergent gene expression profiles of ThPOK-dependent autoregulatory loop disrupted in CD4 T cells.

2021-04-05 | GSE168770 | GEO

Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function [ATAC-seq]

Project description:The transcription factor ThPOK is critical for homeostasis and differentiation of mature T helper cells. Overall goal of this experiment is to show divergent Chromatin pattern of ThPOK-dependent autoregulatory loop disrupted in CD4 T cells compared to WT.

2021-04-05 | GSE168771 | GEO

Genome-wide maps of Bcl11b bound regions in thymocytes

Project description:T-cell receptor (TCR) signals play a critical role in guiding selected thymocytes to distinct lineages by activating genes for transcription factors, such as ThPOK and Runx3, for the helper- or cytotoxic-lineage, respectively. Here we show that Bcl11b, known as an early T-lineage commitment factor, is essential for proper expression of ThPOK and Runx3. Loss of Bcl11b resulted in premature and random expression of these specification factors, leading to lineage scrambling that was disconnected from TCR restriction by MHC. Early Thpok repression by Bcl11b is independent of its known transcriptional silencer, but requires the C-terminal zinc-finger of Bcl11b. Collectively, our findings shed new light on the role of Bcl11b in priming lineage-specifying genes to integrate TCR signals into a subsequent developmental program that dissects effector lineages.

2017-07-20 | GSE90949 | GEO

An Integrated Epigenomic and Transcriptomic Map of Mouse and Human ab T Cell Development (Thpok ChIPSeq)

Project description:ab lineage T cells, most of which are CD4+ or CD8+ and recognize MHC I or MHC II-presented antigens, are essential for immune responses and develop from CD4+CD8+ thymocytes. The absence of in vitro models and the heterogeneity of ab thymocytes have hampered analyses of their intrathymic differentiation. Here, combining single-cell RNA and ATAC (chromatin accessibility) sequencing, we identified mouse and human ab thymocyte developmental trajectories. We demonstrated asymmetric emergence of CD4+ and CD8+ lineages, matched differentiation programs of agonist-signaled cells to their MHC specificity, and identified correspondences between mouse and human transcriptomic and epigenomic patterns. Through computational analysis of single-cell data and binding sites for the CD4+ lineage transcription factor Thpok, we inferred transcriptional networks associated with CD4+ or CD8+ lineage differentiation, and with expression of Thpok or of the CD8+ lineage factor Runx3. Our findings provide insight into the mechanisms of CD4+ and CD8+ T cell differentiation and a foundation for mechanistic investigations of ab T cell development.

2020-11-25 | GSE148976 | GEO

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