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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE168771 | GEO | 2021/04/05

REPOSITORIES: GEO

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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.

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Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function

Project description:Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function

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Essential role of a ThPOK autoregulatory loop in the maintenance of mature CD4<sup>+</sup> T cell identity and function.

Project description:The transcription factor ThPOK (encoded by the Zbtb7b gene) controls homeostasis and differentiation of mature helper T cells, while opposing their differentiation to CD4+ intraepithelial lymphocytes (IELs) in the intestinal mucosa. Thus CD4 IEL differentiation requires ThPOK transcriptional repression via reactivation of the ThPOK transcriptional silencer element (SilThPOK). In the present study, we describe a new autoregulatory loop whereby ThPOK binds to the SilThPOK to maintain its own long-term expression in CD4 T cells. Disruption of this loop in vivo prevents persistent ThPOK expression, leads to genome-wide changes in chromatin accessibility and derepresses the colonic regulatory T (Treg) cell gene expression signature. This promotes selective differentiation of naive CD4 T cells into GITRloPD-1loCD25lo (Triplelo) Treg cells and conversion to CD4+ IELs in the gut, thereby providing dominant protection from colitis. Hence, the ThPOK autoregulatory loop represents a key mechanism to physiologically control ThPOK expression and T cell differentiation in the gut, with potential therapeutic relevance.

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

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

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

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

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Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function

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

2021-04-05 | GSE168772 | 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

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.

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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

Gene expression in mature CD4 and CD8 from WT mice and mature CD4 from DBTBLZ or Mta2-DBTBLZ retrogenic mice

Project description:T cell precursors develop into cytotoxic CD8 and helper CD4+ T cells in thymus. Thpok, a BTB/POZ family transcription factor, enforces commitment to the CD4 lineage and suppresses cytotoxic gene expression. However, it is still not fully understood how Thpok directs CD4 T cell development. Here, using mass-spectrometry, we identify nucleosome remodeling and deacetylase (NuRD) complex as a novel Thpok cofactor. We demonstrate that the Thpok BTB domain is essential for NuRD recruitment. Reconstituting NuRD binding to a BTB-less version of Thpok (which cannot bind NuRD) restored CD4 T cell in vivo. RNA sequencing showed that CD4 T cells expressing the reconstituted protein express a transcriptome similar to that of CD4 T cells expressing Thpok. Thus, our results demonstrate that NuRD recruitment is both necessary and sufficient for the function of the Thpok BTB domain in CD4 T cell development.

2022-06-10 | GSE171610 | GEO

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