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T cell-specific P2RX7 favors lung parenchymal CD4+ T cell accumulation in response to severe lung infections

ABSTRACT: T cell-specific P2RX7 favors lung parenchymal CD4+ T cell accumulation in response to severe lung infections

PROVIDER: PRJNA1021635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26197721_1.fastq.gz	Fastqsanger.gz
	SRR26197721_2.fastq.gz	Fastqsanger.gz
	SRR26197722_1.fastq.gz	Fastqsanger.gz
	SRR26197722_2.fastq.gz	Fastqsanger.gz
	SRR26197723_1.fastq.gz	Fastqsanger.gz

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T cell-specific P2RX7 favors lung parenchymal CD4+ T cell accumulation in response to severe lung infections

Project description:CD4+ T cells are key components of the immune response during lung infections and can mediate protection against tuberculosis (TB) or influenza. However, CD4+ T cells can also promote lung pathology during these infections, making it unclear how these cells control such discrepant effects. Using mouse models of hypervirulent TB and influenza, we observed that exaggerated accumulation of parenchymal CD4+ T cells promotes lung damage. Low numbers of lung CD4+ T cells, in contrast, are sufficient to protect against hypervirulent TB. In both situations, lung CD4+ T cell accumulation is mediated by CD4+ T cell-specific expression of the extracellular ATP (eATP) receptor P2RX7. P2RX7 upregulation in lung CD4+ T cells promotes expression of the chemokine receptor CXCR3 and favors in situ proliferation. Our findings suggest that direct sensing of lung eATP by CD4+ T cells is critical to induce tissue CD4+ T cell accumulation and pathology during lung infections.

2024-02-14 | GSE244194 | GEO

T cell-specific P2RX7 favors lung parenchymal CD4<sup>+</sup> T cell accumulation in response to severe lung infections.

Project description:CD4+ T cells are key components of the immune response during lung infections and can mediate protection against tuberculosis (TB) or influenza. However, CD4+ T cells can also promote lung pathology during these infections, making it unclear how these cells control such discrepant effects. Using mouse models of hypervirulent TB and influenza, we observe that exaggerated accumulation of parenchymal CD4+ T cells promotes lung damage. Low numbers of lung CD4+ T cells, in contrast, are sufficient to protect against hypervirulent TB. In both situations, lung CD4+ T cell accumulation is mediated by CD4+ T cell-specific expression of the extracellular ATP (eATP) receptor P2RX7. P2RX7 upregulation in lung CD4+ T cells promotes expression of the chemokine receptor CXCR3, favoring parenchymal CD4+ T cell accumulation. Our findings suggest that direct sensing of lung eATP by CD4+ T cells is critical to induce tissue CD4+ T cell accumulation and pathology during lung infections.

| S-EPMC10841667 | biostudies-literature

Expression data of ex vivo purified CD4+ cells from WT and P2rx7-/- mice

Project description:Extracellular adenosine triphosphate (eATP) is a signaling molecule that affects T cell function via the ionotropic P2X7 receptor. The study of effector/memory T cells isolated from mice with deletion of P2rx7, the gene encoding for P2X7, allowed understanding the impact of P2X7 activity on T cell function in the eATP-rich tumor microenvironment. To explore the the transcriptional impact of the lack of P2rx7 in CD4+ naïve and TEM cells, we performed genome-wide expression profiling of ex vivo purified CD4+ naïve and TEM cells from WT and P2rx7-/- mice

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Tet1 and Tet2 Maintain Mesenchymal Stem Cell Homeostasis via demethylation of P2rX7 promoter

Project description:Ten-eleven translocation (Tet) family-mediated DNA oxidation represents a novel epigenetic modification capable of converting 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC) to regulate various biological processes. However, it is unknown whether the Tet family affects mesenchymal stem cells (MSCs) or the skeletal system. Here we show that depletion of Tet1 and Tet2 resulted in impaired self-renewal and differentiation of bone marrow MSCs (BMMSCs) and a significant osteopenia phenotype. Mechanistically, Tet1 and Tet2 deficiency reduced demethylation of the P2rX7 promoter and thus downregulated exosome release, leading to intracellular accumulation of miR-297a-5p, miR-297b-5p, and miR-297c-5p. These miRNAs inhibited Runx2 signaling to impair BMMSC function. We show that overexpression of P2rX7 consistently rescued the impaired BMMSCs and osteoporotic phenotype in Tet1 and Tet2 double knockout mice. These results indicate that Tet1 and Tet2 play a critical role in maintaining BMMSC and bone homeostasis through epigenetic regulation of P2rX7 to control exosome and miRNA release. This newly identified Tet/P2rX7/Runx2 cascade may serve as a target for the development of novel therapies for osteopenia disorders.

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mRNA expression profiling after Ago2-immunoprecipitation (IP) in unstimulated and TGF-β1-stimulated primary parenchymal lung fibroblasts of two control subjects

Project description:To identify the target gene repertoire of miRNAs (i.e. the miRNA-targetome) of unstimulated and TGF-β1-stimulated primary parenchymal lung fibroblasts, Ago2-IP was performed followed by mRNA expression profiling.

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RNA-seq comparison of whole muscle between WT mice, dystrophic mice, and P2rx7-null dystrophic mice

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2019-09-26 | E-MTAB-7698 | biostudies-arrayexpress

DNA methylation in airway and parenchymal fibroblasts isloated by from individuals with and without asthma

Project description:Background: Mesenchymal fibroblasts are ubiquitous cells that maintain the extracellular matrix of organs. Within the lung, airway and parenchymal fibroblasts are crucial for lung development and are altered with disease, but it has been difficult to understand their roles due to the lack of distinct molecular markers.

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Sequence-specific targeting of dosage compensation in Drosophila favors an active chromatin context

Project description:This SuperSeries is composed of the following subset Series: GSE34857: Sequence-specific targeting of dosage compensation in Drosophila favors an active chromatin context (ChIP-chip) GSE34858: Sequence-specific targeting of dosage compensation in Drosophila favors an active chromatin context (mRNA) Refer to individual Series

2012-03-19 | E-GEOD-34859 | biostudies-arrayexpress

Regulatory function of Pja2 mediated by the P2rx3/P2rx7 axis in mouse hippocampal neuronal cells

Project description:Praja2 (Pja2), a member of the growing family of mammalian RING E3 ubiquitin ligases, is reportedly involved not only in several types of cancer but also in neurological diseases and disorders. However, the underlying genetic mechanism of Pja2 regulation in the nervous system remains unclear. To study the cellular and molecular function of Pja2 in mouse hippocampal neuronal cells (MHNCs), we used gain- and loss-of-function manipulations of Pja2 in HT-22 cells and tested their regulatory effects on three Alzheimer's disease (AD) genes and cell proliferation. We found that the expression of AD markers including App, Mapt and Gsap could be inhibited by Pja2 overexpression and activated by Pja2 knockdown. In addition, HT-22 cell proliferation was enhanced by Pja2 upregulation and suppressed by its downregulation. We also applied RNA-Seq to evaluate and quantify the targets that responded to the enforced expression of Pja2. In particular, P2rx3 and P2rx7, which have different expression patterns in the critical calcium signaling pathway, were shown to mediate the regulatory effect of Pja2 in HT-22 cells. Functional studies indicated that Pja2 regulated HT-22 cell development and AD marker genes by inhibiting P2rx3 but promoting P2rx7, a gene downstream of P2rx3. In conclusion, our results provide new insights into the regulatory function of the gene Pja2 in MHNCs, underscoring the potential relevance of this molecule to the pathophysiology of AD.

2020-12-15 | E-MTAB-6464 | biostudies-arrayexpress

TAK1 deficient liver parenchymal cells with Rip3 double knockout TAK1LPC

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