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Thymic development of type-17 innate-like T cells depends on PTEN

ABSTRACT: Thymic development of type-17 innate-like T cells depends on PTEN

PROVIDER: PRJNA744084 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR15048901_1.fastq.gz	Fastqsanger.gz
	SRR15048901_2.fastq.gz	Fastqsanger.gz
	SRR15048902_1.fastq.gz	Fastqsanger.gz
	SRR15048902_2.fastq.gz	Fastqsanger.gz

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Thymic development of type-17 innate-like T cells depends on a PTEN-coordinated two-step process linking TCR and IL-23–IL-23R–Stat3 axis

Project description:PTEN orchestrates a two-step process downstream of TCR and IL-23–Stat3 signaling to control type-17 innate-like T cell generation. Complete or partial deletion of PTEN led to the massive and selective accumulation of IL-17-producing thymocytes We used microarrays to compare the global transcription profiles of WT, Cd4CrePtenfl/fl, and Cd4CrePten+/fl thymocyte population

2022-10-04 | GSE152294 | GEO

Thymic development of type-17 innate-like T cells depends on a PTEN-coordinated two-step process linking TCR and IL-23–IL-23R–Stat3 axis

Project description:Thymic development of type-17 innate-like T cells depends on a PTEN-coordinated two-step process linking TCR and IL-23–IL-23R–Stat3 axis

| PRJNA638917 | ENA

Thymic development of type-17 innate-like T cells depends on PTEN

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

2022-10-04 | GSE179512 | GEO

Biallelic and complicated inactivation of Pten in radiation-induced mouse thymic lymphomas

Project description:Inactivation of Pten occurs by multiple mechanisms including epigenetic silencing, point mutations, insertion, and deletion, which are tissue dependent. Although frequent loss of heterozygosity around Pten locus and plausible involvement of epigenetic silencing have been reported in radiation-induced thymic lymphomas, the frequency of Pten inactivation and the spectrum of causal aberrations have not yet been extensively characterized. Here, we assessed the principal mode of inactivation by comprehensively analyzing expression and alterations of Pten gene in 23 radiation-induced thymic lymphomas developed in B6C3F1 mice. We found no evidence for methylation-associated silencing of Pten gene. Instead, we found complex structural abnormalities in 8 lymphomas (35%) that included missense and nonsense mutations, 1- and 3-bp insertions, and focal deletions. Sequencing of deletion breakpoints suggested that illegitimate V(D)J recombination and microhomology-mediated rearrangement were responsible for the focal deletions. Seven out of these 8 lymphomas had biallelic alterations, and 4 of them did not express any Pten protein. These aberrations of Pten were well coincided with downstream Akt phosphorylation on Ser473. In conclusion, Pten inactivation, which is frequently biallelic and is caused by a variety of structural abnormalities but not by epigenetic silencing, is involved in radiation-induced lymphomagenesis. Three thymic lymphomas were analyzed by array-CGH method.

2010-05-06 | E-GEOD-17751 | biostudies-arrayexpress

Biallelic and complicated inactivation of Pten in radiation-induced mouse thymic lymphomas

2010-03-01 | GSE17751 | GEO

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 [Stat3KO 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 | GSE206462 | GEO

Evaluation of effect of PTEN gene deletion in mouse CD4+ Th1 clones after stimulation

Project description:PTEN is thought to play a critical role in T cell activation by negatively regulating the PI3K signaling pathway important for cellular activation, growth, and proliferation. T cells from mice in which PTEN was conditionally deleted in the thymus were reported to display CD28-independent IL-2 production and relative resistance to anergy induction. However, such observations could have stemmed from alterations in T cell development due to early deletion in thymocytes. To directly eliminate PTEN in post-thymic T cells, we utilized CAR Tg x PTENflox/flox mice which enabled gene deletion using a Cre adenovirus in vitro. Gene expression profiling revealed a small subset of induced genes that were augmented upon PTEN deletion and T cell stimulation. Our results indicate that deletion of PTEN can augment the activation of post-thymic T cells. Nonetheless, PTEN inhibition may be a viable target for immune potentiation due to increased cytokine production by activated CD4+ cells. It was of interest to determine the spectrum of transcripts regulated by PTEN using gene expression profiling. To this end, CAR Tg x PTENflox/flox Th1 clones were either treated with adeno-Cre or adeno-EV, then confirmed to have PTEN protein abscence by western blot, then stimulated for 6 hours with anti-CD3/anti-CD28 mAb- coated beads and analyzed (2 total conditions). The experiment was replicated so there are 2 samples for each condition.

2013-02-01 | E-GEOD-43936 | biostudies-arrayexpress

Evaluation of effect of PTEN gene deletion in mouse CD4+ Th1 clones after stimulation

2013-02-01 | GSE43936 | GEO

Innate to adaptive: Human IFN-gamma producing CD4+ T cells can derive directly from CXCL8-producing recent thymic emigrants.

Project description:An unanticipated feature of the human neonatal CD4 T cell response is a robust capacity to produce CXCL8. However, this 'innate-like' function dissipates with age and is scarce in the adult. Here, we investigated the fate of CD4+CXCL8+ cells and their transition into conventional adaptive T cells. We show that CXCL8 is imprinted on immature thymocytes prior to TCR signalling and is maintained in T cell committed thymic progenitors and recent thymic emigrants (RTEs) of adults as well as neonates. Hence, rather than being unique to neonates, CXCL8-producing CD4+ T cells decrease with age in humans (and in humanised mice) owing to the decline in thymic output, coupled with the cells’ peripheral expansion. By cloning of CXCL8+CD4+ cells from cord blood, we were able to track effector function within daughter cells and demonstrate that these cells can convert to IFN-g producing cells. In sum, we provide direct evidence that ‘innate like’ CXCL8-producing CD4+ T cells emerge from the thymus and can transition into conventional adaptive Th1 cells

2017-08-09 | GSE84686 | GEO

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