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Differentiation and homeostasis of effector Treg cells are regulated by inositol polyphosphates modulating Ca2+ influx

ABSTRACT: Differentiation and homeostasis of effector Treg cells are regulated by inositol polyphosphates modulating Ca2+ influx

PROVIDER: PRJNA817570 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18366613.fastq.gz	Fastqsanger.gz
	SRR18366614.fastq.gz	Fastqsanger.gz
	SRR18366615.fastq.gz	Fastqsanger.gz
	SRR18366616.fastq.gz	Fastqsanger.gz
	SRR18366617.fastq.gz	Fastqsanger.gz

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Differentiation and homeostasis of effector Treg cells are regulated by inositol polyphosphates modulating Ca2+ influx

Project description:Activated Foxp3+ regulatory T (Treg) cells differentiate into effector Treg (eTreg) cells to maintain peripheral immune homeostasis and tolerance. T cell receptor (TCR)-mediated induction and regulation of store-operated Ca2+ entry (SOCE) is essential for eTreg cell differentiation and function. However, SOCE regulation in Treg cells remains unclear. Here we show that inositol polyphosphate multikinase (IPMK), which generates inositol tetrakisphosphate and inositol pentakisphosphate, is a pivotal regulator of Treg cell differentiation downstream of TCR signaling. IPMK is highly expressed in TCR-stimulated Treg cells and promotes a TCR-induced Treg cell program. IPMK-deficient Treg cells display aberrant T cell activation and impaired differentiation into RORγt+ Treg cells, and tissue-resident Treg cells. Mechanistically, IPMK controls the generation of higher-order inositol phosphates, thereby promoting Ca2+ mobilization and Treg cell effector functions. Our findings identify IPMK as a critical regulator of TCR-mediated Ca2+ influx and highlight the importance of IPMK in Treg cell-mediated immune homeostasis.

2023-05-18 | GSE198960 | GEO

Differentiation and homeostasis of effector Treg cells are regulated by inositol polyphosphates modulating Ca<sup>2+</sup> influx.

Project description:Activated Foxp3+ regulatory T (Treg) cells differentiate into effector Treg (eTreg) cells to maintain peripheral immune homeostasis and tolerance. T cell receptor (TCR)-mediated induction and regulation of store-operated Ca2+ entry (SOCE) is essential for eTreg cell differentiation and function. However, SOCE regulation in Treg cells remains unclear. Here, we show that inositol polyphosphate multikinase (IPMK), which generates inositol tetrakisphosphate and inositol pentakisphosphate, is a pivotal regulator of Treg cell differentiation downstream of TCR signaling. IPMK is highly expressed in TCR-stimulated Treg cells and promotes a TCR-induced Treg cell program. IPMK-deficient Treg cells display aberrant T cell activation and impaired differentiation into RORγt+ Treg cells and tissue-resident Treg cells. Mechanistically, IPMK controls the generation of higher-order inositol phosphates, thereby promoting Ca2+ mobilization and Treg cell effector functions. Our findings identify IPMK as a critical regulator of TCR-mediated Ca2+ influx and highlight the importance of IPMK in Treg cell-mediated immune homeostasis.

| S-EPMC9271192 | biostudies-literature

Ca2+ influx through ORAI1 and ORAI2 channels regulates chromatin accessibility in CD4+ T cells

Project description:Activation of CD4+ T cells by T cell receptor (TCR) signaling results in altered gene expression as a result of epigenetic and transcriptional regulation. A critical TCR signaling pathway in CD4+ T cells is driven by Ca2+ influx across the plasma membrane through Ca2+ release-activated Ca2+ (CRAC) channels that are formed by ORAI1 and ORAI2 proteins. Here we analyzed the effects of suppressing Ca2+ influx in mouse CD4+ T cells on chromatin accessibility by genetically deleting the ORAI1 channel alone or both ORAI1 and ORAI2 channels. CD4+ T cells specific for ovalbumin (OVA) from TCR transgenic OT-II were activated by in vivo exposure to influenza A virus (IAV) expressing OVA neoantigen. Changes in chromatin accessibility of CD4+ T cells in response to IAV-OVA infection were determined by ATAC sequencing

2025-01-01 | GSE253187 | GEO

TRPV6 essentially contributes to Ca2+ influx in endometrial epithelial cells and female mouse fecundity

Project description:The Ca2+-selective transient receptor potential vanilloid 6 (TRPV6) channel plays a fundamental role in the mouse female and male reproductive system. In mouse endometrium the TRPV6 protein is highly expressed in epithelial cells (MEECs). Using Ca2+ imaging and patch clamp analysis we found that TRPV6 contributes to the cytosolic Ca2+ level, more specifically to the Ca2+ influx into the MEECs. As compared to wild-type cells, Trpv6-deficient MEECs reveal a significantly reduced frequency of spontaneous cytosolic Ca2+ oscillations, shown in both isolated cells and the complete uterus in situ. Noteworthy, in MEECs we here show for the first time distinct endogenous TRPV6-dependent whole-cell currents detected from primary cells. Our results disclose a previously unknown physiological role for TRPV6 in the regulation of endometrial Ca2+ homeostasis and its impact on female mouse fecundity, representing a basis for further investigation of reproductive impairments e.g. associated with defective Ca2+ regulation in women.

2025-10-13 | PXD060418 | Pride

Transcriptome analysis of cryptococcal IPK mutants

Project description:In eukaryotes, inositol polyphosphates perform essential metabolic and signaling functions. Using human fungal pathogen Cryptococcus neoformans as a model, we created mutants in three inositol polyphosphates kinases: Arg1, Ipk1 and Kcs1. Each of the mutants produces a unique repertoire of inositol polyphosphates, different from the wild type strain. Comparative phenotypic and transcriptome analyses of wild type and mutant strains indicates that inositol polyphosphate PP-IP5 (IP7) is the key regulator of gene expression, fitness and virulence in C. neoformans.

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Transcriptome analysis of cryptococcal IPK mutants

2016-03-03 | E-GEOD-78824 | biostudies-arrayexpress

Ca2+ influx through ORAI1 and ORAI2 channels regulates chromatin accessibility in CD4+ T cells

Project description:Ca2+ influx through ORAI1 and ORAI2 channels regulates chromatin accessibility in CD4+ T cells

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Fight or flight cardiac responses require augmentation of Ca2+ influx via Rad phosphorylation [RNAseq]

Project description:Fight or flight cardiac responses require augmentation of Ca2+ influx via Rad phosphorylation [RNAseq]

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Circ-CAMTA1 regulated by Ca2+ influx inhibited pyruvate carboxylase activity and modulate T cell function in patients with systemic lupus erythematosus

Project description:The expression profiles of circRNAs in Jurkats cells, co-cultured with and without ionomycin, were analyzed by next-generation sequencing and validated using real-time polymerase chain reaction. The identified Ca2+ influx-regulated circRNAs were further examined in T cells from 42 patients with SLE and 23 healthy controls. The biological function of specific circRNAs was investigated using transfection and RNA pull-down assay. After validation, we confirmed that the expression levels of circ-ERCC4, circ-NFATC2, circ-MYH10, circ-CAMTA1, circ-ASH1L, circ-SOCS7, and circ-ASAP1 were consistently increased in Jurkat cells following Ca2+ influx. The expression levels of circ-CAMTA1, circ-ASH1L, and circ-ASAP1 were significantly lower in T cells from patients with SLE, with even lower levels observed in those with higher disease activity. Interferon (IFN)-α was found to suppress the expression of circ-CAMTA1. Circ-CAMTA1 bound to pyruvate carboxylase and inhibited its biologic activity. Overexpression of circ-CAMTA1, but not its linear form, significantly decreased extracellular glucose levels. Furthermore, increased expression of circ-CAMTA1, but not its linear form, enhanced IL-2 secretion and the protein expression of NFAT1.

2024-11-06 | GSE278650 | GEO

Effect of polyphosphates on osteoblast mineralization

Project description:Rat osteoblasts ROB17/2.8 cells were cultured in the presence of high (1mg/ml) or low (0.01mg/ml) concentration of polyphosphates.

2016-03-15 | GSE79176 | GEO

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