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PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Stat3KO rescue]

ABSTRACT: Developmental and metabolic signaling networks underpinning type-17 cell fate decisions and functional effects at coordination of PTEN-dependent tissue homeostasis

ORGANISM(S): Mus musculus

PROVIDER: GSE206462 | GEO | 2022/10/04

REPOSITORIES: GEO

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PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Raptor_or_Rictor_KO_rescue]

Project description:Developmental and metabolic signaling networks underpinning type-17 cell fate decisions and functional effects at coordination of PTEN-dependent tissue homeostasis

2022-10-04 | GSE206467 | GEO

PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [scRNA-seq and scTCR-seq Exp2]

Project description:Developmental and metabolic signaling networks underpinning type-17 cell fate decisions in dictating tissue homeostasis versus tissue homeostasis

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Metabolic reprogramming of innate-like T cell fate and tissue homeostasis by PTEN [scRNA- and scTCR-seq]

Project description:Developmental and metabolic signaling networks underpinning type-17 cell fate decisions in dictating tissue homeostasis versus fatal autoimmunity

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PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Stat3KO rescue]

Project description:PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Stat3KO rescue]

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PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Raptor_or_Rictor_KO_rescue]

Project description:PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Raptor_or_Rictor_KO_rescue]

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PTEN directs developmental and metabolic signaling for innate-like T cell fate and tissue homeostasis.

Project description:Phosphatase and tensin homologue (PTEN) is frequently mutated in human cancer, but its roles in lymphopoiesis and tissue homeostasis remain poorly defined. Here we show that PTEN orchestrates a two-step developmental process linking antigen receptor and IL-23-Stat3 signalling to type-17 innate-like T cell generation. Loss of PTEN leads to pronounced accumulation of mature IL-17-producing innate-like T cells in the thymus. IL-23 is essential for their accumulation, and ablation of IL-23 or IL-17 signalling rectifies the reduced survival of female PTEN-haploinsufficient mice that model human patients with PTEN mutations. Single-cell transcriptome and network analyses revealed the dynamic regulation of PTEN, mTOR and metabolic activities that accompanied type-17 cell programming. Furthermore, deletion of mTORC1 or mTORC2 blocks PTEN loss-driven type-17 cell accumulation, and this is further shaped by the Foxo1 and Stat3 pathways. Collectively, our study establishes developmental and metabolic signalling networks underpinning type-17 cell fate decisions and their functional effects at coordinating PTEN-dependent tissue homeostasis.

| S-EPMC10080469 | biostudies-literature

Non-apoptotic Fas signaling controls CD40 dependent mTOR activation and human B cell fate via PTEN nuclear exclusion

Project description:Defective Fas signaling causes autoimmune lymphoproliferative syndrome (ALPS). While defective apoptosis may impair negative selection and removal of autoreactive B lymphocytes, Fas transmits also non-apoptotic signals. We show herethat transient Fas ligation in CD40L-stimulated human B cells specifically decreased the mTOR axis activation without causing apoptosis. This signal modulation was absent in ALPS patients. Rather, mTOR signaling was enhanced in germinal center (GC) B cells and plasmablasts derived from a ALPS patient lymph node . Mechanistically, transient Fas engagement induced recruitment of DAXX to the activated Fas complex and nuclear exclusion of PTEN. Likewise, Fas stimulation promoted expression of transcripts like MYC and CXCR4, that regulate GC formation and fate decisions of established GC B cells. We suggest that non-apoptotic Fas signaling has a physiological impact on activated B cell fate decisions explaining the effectiveness of mTOR inhibitors in the treatment of ALPS autoimmunity.

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PLEKHS1 drives PI3Ks and remodels pathway homeostasis in PTEN-null prostate

Project description:The PIP3/PI3K network is a central regulator of metabolism and is frequently activated in cancer, commonly by loss of the PIP3/PI(3,4)P2-phosphatase, PTEN. Despite huge investment, the drivers of the PI3K network in normal tissues and how they adapt to overactivation are unclear. We find that in healthy mouse prostate PI3K activity is driven by RTK/IRS signalling and constrained by pathway-feedback. In the absence of PTEN, the network is dramatically remodelled. A poorly understood, YXXM- and PIP3/PI(3,4)P2-binding PH domain-containing, adaptor, PLEKHS1, became the dominant activator and was required to sustain PIP3, AKT-phosphorylation and growth in PTEN-null prostate. This was because PLEKHS1 evaded pathway-feedback and experienced enhanced PI3K- and SRC-family kinase-dependent phosphorylation of Y258XXM, eliciting PI3K-activation. hPLEKHS1-mRNA and activating-Y419-phosphorylation of hSRC correlated with PI3K-pathway activity in human prostate cancers. We propose that in PTEN-null cells, receptor-independent, SRC-dependent tyrosine-phosphorylation of PLEKHS1 creates positive-feedback that escapes homeostasis, drives PIP3-signalling and supports tumour progression.

2023-08-23 | PXD043239 | Pride

PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [scRNA-seq and scTCR-seq Exp2]

Project description:PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [scRNA-seq and scTCR-seq Exp2]

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Metabolic reprogramming of innate-like T cell fate and tissue homeostasis by PTEN [scRNA- and scTCR-seq]

Project description:Metabolic reprogramming of innate-like T cell fate and tissue homeostasis by PTEN [scRNA- and scTCR-seq]

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