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The Transcription Factor ThPOK Regulates ILC3 Lineage Homeostasis and Function during Intestinal Infection

ABSTRACT: The Transcription Factor ThPOK Regulates ILC3 Lineage Homeostasis and Function during Intestinal Infection

PROVIDER: PRJNA839935 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19330091.fastq.gz	Fastqsanger.gz
	SRR19330092.fastq.gz	Fastqsanger.gz
	SRR19330093.fastq.gz	Fastqsanger.gz
	SRR19330094.fastq.gz	Fastqsanger.gz
	SRR19330095.fastq.gz	Fastqsanger.gz

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The Transcription Factor ThPOK Regulates ILC3 Lineage Homeostasis and Function during Intestinal Infection

Project description:To investigate the role of ThPOK in the regulation of ILC3 development and function, we established conventional ThPOK knockout mice.

2022-05-23 | GSE203422 | GEO

The Transcription Factor ThPOK Regulates ILC3 Lineage Homeostasis and Function during Intestinal Infection II

Project description:To investigate the role of ThPOK in the regulation of ILC3 development and function, we established conventional ThPOK knockout mice and carried out single-cell RNA sequencing (BD Rhapsody) on intestinal ILC3s.

2022-06-28 | GSE204698 | GEO

The Transcription Factor ThPOK Regulates ILC3 Lineage Homeostasis and Function during Intestinal Infection II

Project description:The Transcription Factor ThPOK Regulates ILC3 Lineage Homeostasis and Function during Intestinal Infection II

| PRJNA841977 | ENA

The Transcription Factor ThPOK Regulates ILC3 Lineage Homeostasis and Function During Intestinal Infection.

Project description:Innate lymphoid cells (ILCs) have been identified as a heterogeneous population of lymphocytes that mirrors the cytokine and transcriptional profile of adaptive T cells. The dynamic balance between key transcription factors determines the heterogeneity, plasticity, and functions of ILC subsets. The transcription factor ThPOK is highly conserved in biological evolution and exerts pivotal functions in the differentiation of T cells. However, the function of ThPOK in ILC3s has not been identified. Here, we found that ThPOK regulated the homeostasis of ILC3s, as mice lacking ThPOK showed decreased NKp46+ ILC3s and increased CCR6- NKp46- ILC3s. ThPOK-deficient mice were more sensitive to S. typhimurium infection due to the impaired IFN-γ secretion of NKp46+ ILC3s. Furthermore, ThPOK participates in ILC3-mediated control of C. rodentium infection by negatively regulating IL-17A secretion. ThPOK preserves the identity of NKp46+ ILC3s by repressing RORγt, which indirectly releases T-bet expression. On the molecular level, ThPOK directly binds to Rorc and Il23r to restrain their expression which further modulates IL-17A secretion. Collectively, our analysis revealed a critical role of ThPOK in the homeostasis and functions of ILC3 subsets.

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PD-1 regulates ILC3-driven intestinal immunity and homeostasis

Project description:PD-1 regulates ILC3-driven intestinal immunity and homeostasis

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PD-1 regulates ILC3-driven intestinal immunity and homeostasis

Project description:PD-1 is constitutively expressed on a fraction of ILC3 in the gut. To identify the transcriptional differences between PD1+ and PD1- ILC3, we have sorted these subsets and analysed their transcriptional regulation by RNA-Seq.

2024-02-29 | GSE254794 | GEO

NuRD complex recruitment to Thpok mediates CD4+ T cell lineage differentiation

Project description:Although BTB-zinc finger (BTB-ZF) transcription factors control the differentiation of multiple hematopoietic and immune lineages, how they function is poorly understood. The BTB-ZF factor Thpok controls intrathymic CD4+ T cell development and expression of most CD4+- and CD8+-lineage genes. Here, we identify the nucleosome remodeling and deacetylase (NuRD) complex as a novel Thpok cofactor. We locate three amino-acid residues within the Thpok BTB domain that are required for both NuRD binding and Thpok functions, and show that NuRD recruitment recapitulates the functions of the Thpok BTB domain. NuRD mediates Thpok repression of CD8+-lineage genes, including the transcription factor Runx3, but is dispensable for Cd4 expression. We show that these functions cannot be performed by the BTB domain of the Thpok-related factor Bcl6, which fails to bind NuRD. Thus, cofactor binding critically contributes to the functional specificity of BTB-zinc finger factors, which control the differentiation of most hematopoietic subsets.

2022-06-10 | GSE199739 | GEO

Light-entrained and brain-tuned circadian circuits regulate ILC3 and gut homeostasis

Project description:Group 3 innate lymphoid cells (ILC3) are major regulators of inflammation, infection, microbiota composition and metabolism. ILC3 and neuronal cells were shown to interact at discrete mucosal locations to steer mucosal defence. Nevertheless, whether neuroimmune circuits operate at an organismal level, integrating extrinsic environmental signals to orchestrate ILC3 responses remains elusive. Here we show that light-entrained and brain-tuned circadian circuits regulate enteric ILC3, intestinal homeostasis and the host lipid metabolism. We found that enteric ILC3 display circadian expression of clock genes and ILC3-related transcription factors. ILC3-autonomous ablation of the circadian regulator Arntl led to disrupted gut ILC3 homeostasis, impaired epithelial reactivity, deregulated microbiome, increased susceptibility to bowel infection and disrupted lipid metabolism. Loss of ILC3-intrinsic Arntl shaped the gut postcode receptors of ILC3. Strikingly, light-dark cycles, feeding rhythms and microbial cues differentially regulated ILC3 clocks, with light signals as major entraining cues of ILC3. Accordingly, surgical- and genetically-induced deregulation of brain rhythmicity led to disrupted circadian ILC3 oscillations, deregulated microbiome and altered lipid metabolism. Our work reveals a circadian circuitry that translates environmental light cues into enteric ILC3, shaping intestinal health and organismal homeostasis.

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ThPOK is a critical and multifaceted regulator of myeloid lineage development [Fluidigm]

Project description:The transcription factor ThPOK (encoded by Zbtb7b) is well known for its role as a master regulator of CD4 lineage commitment in the thymus. Here, we report a novel role for ThPOK as a critical and multifaceted regulator of myeloid lineage commitment, differentiation and maturation. Using reporter and knockout mouse models combined with CITE-Seq, Smart-Seq2, progenitor transfer and clonogenic assays and we show that ThPOK controls monocyte-DC versus granulocyte lineage production during homeostatic differentiation, and serves as a brake for neutrophil maturation in granulocyte lineage-specified cells through transcriptional regulation of lineage-specific transcription factors and RNA via altered mRNA splicing to reprogram intron retention.

2023-06-05 | GSE163843 | GEO

ThPOK is a critical and multifaceted regulator of myeloid lineage development [CITE-Seq]

2023-06-05 | GSE163837 | GEO