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Co-expression of IL-15 and CCL21 strengthens CAR-NK cells to eliminate tumors in concert with T cells and equips them with enhanced PI3K/AKT/mTOR signal signature

ABSTRACT: Co-expression of IL-15 and CCL21 strengthens CAR-NK cells to eliminate tumors in concert with T cells and equips them with enhanced PI3K/AKT/mTOR signal signature

PROVIDER: PRJNA1167653 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30851201_1.fastq.gz	Fastqsanger.gz
	SRR30851201_2.fastq.gz	Fastqsanger.gz
	SRR30851202_1.fastq.gz	Fastqsanger.gz
	SRR30851202_2.fastq.gz	Fastqsanger.gz
	SRR30851203_1.fastq.gz	Fastqsanger.gz

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Co-expression of IL-15 and CCL21 strengthens CAR-NK cells to eliminate tumors in concert with T cells and equips them with enhanced PI3K/AKT/mTOR signal signature

Project description:Chimeric antigen receptor (CAR) natural killer (NK) cell therapy has demonstrated safety and feasibility in clinic; yet, limited efficacy resulted from intrinsic dysfunction and extrinsic depression remains to be addressed. T cells provide a multifaceted complementation to NK cell-mediated response. Here, we designed a novel CD19-targeted CAR-NK armored with secreted interleukin (IL) -15 and CCL21 (15x21 CAR-NK) that are capable of recruiting and cooperating with T cells. These 15x21 CAR-NK cells possess excellent capacities for cytotoxicity, cytokine production, and effector molecule expression in vitro. The cooperation with T cells presents benefits of alleviating mutual exhaustion and boosting the expression of effector molecules/receptors, thus promoting the elimination of tumor cells efficiently. In addition, 15x21 CAR-NK cells were also highly enriched PI3K/AKT/mTOR pathway, associating with downstream pro-survival signaling, anti-apoptosis ability, and mitochondrial fitness. Collectively, our study highlights the intrinsic superiority and extrinsic T-cell cooperative advantages of 15x21 CAR-NK cells, providing a promising strategy for NK-cell based immunotherapy.

2025-04-25 | GSE278506 | GEO

RNA-seq of glioblastoma stem cells with CCL21 treatment

Project description:RNA-seq of glioblastoma stem cells with CCL21 treatment

2023-08-04 | GSE178337 | GEO

CCL21 Expression in Beta Cells Induces Antigen-Expressing Stromal Cell Networks in the Pancreas and Prevents Autoimmune Diabetes in Mice

Project description:Tumors induce tolerance towards their antigens by producing the chemokine CCL21, leading to the formation of tertiary lymphoid organs (TLOs). Ins2-CCL21 transgenic, non-obese diabetic (NOD) mice express CCL21 in pancreatic β-cells and do not develop autoimmune diabetes. We investigated by which mechanisms CCL21 expression prevented diabetes. Islet infiltrates of 4 week-old Ins2-CCL21 mice were enriched in naïve CD4+ T cells and compartmentalized within networks of CD45- gp38+ CD31- fibroblastic reticular cell (FRC)-like stromal cells. Importantly, 12 week-old Ins2-CCL21 NOD islets contained FRC-like cells with enhanced expression of β-cell autoantigens and gene expression profiles consistent with regulatory, anti-inflammatory properties and increased contractility. Consistently, transgenic mice harbored fewer autoreactive T cells and higher proportion of Tregs in the islets. Using adoptive transfer and islet transplantation models, we demonstrate that the formation of TLOs in Ins2-CCL21 transgenic islets is critical for regulation of autoimmunity and while the effect is systemic, the induction may be mediated locally by lymphocyte trafficking through TLOs. Overall, our findings suggest that CCL21 promotes TLOs that differ from inflammatory TLOs associated with islets in T1D in that they resemble lymph nodes, contain FRC-like cells expressing β-cell autoantigens and are able to induce systemic and antigen-specific tolerance leading to diabetes prevention. These findings suggest that CCL21 may be exploited for novel immunoregulation approaches to treat autoimmune diabetes.

2019-09-23 | GSE130979 | GEO

RNA-seq of glioblastoma stem cells with CCL21 treatment

Project description:RNA-seq of glioblastoma stem cells with CCL21 treatment

| PRJNA738513 | ENA

HDAC6 inhibitor TST strengthens the antiproliferative effects of PI3K/mTOR inhibitor BEZ235 in breast cancer cells via suppressing RTK activation.

Project description:NVP-BEZ235 (BEZ235), an available dual PI3K/mTOR inhibitor, showed antitumor effect and provided a therapy strategy in carcinomas. However, the acquired upregulation of multiple receptor tyrosine kinases (RTKs) by NVP-BEZ235 in tumors limits its clinical efficacy. HDAC6, a class II histone deacetylase, is associated with expressions of multiple RTKs. The aim of this study was to detect whether co-treatment with HDAC6 inhibitor Tubastatin A (TST) would enhance the anticancer effects of BEZ235 in breast cancer cells. In this study, we described that treatment of breast cancer cell lines (T47D, BT474, and MDA-MB-468) with BEZ235 significantly triggered PI3K/mTOR signaling inactivation and increased multiple RTK expression, including EGFR, HER2, HER3, IGF-1 receptor, insulin receptor, and their phosphorylation levels. The adding of TST destabilized these RTKs in those breast cancer cells. Co-treatment with BEZ235 and TST reduced cell proliferative rate by strengthening Akt inactivation. In addition, the combination of these two drugs also cooperatively arrested cell cycle and DNA synthesis. In conclusion, the co-treatment with PI3K/mTOR inhibitor BEZ235 and HDAC6 inhibitor TST displayed additive antiproliferative effects on breast cancer cells through inactivating RTKs and established a rationable combination therapy to treat breast cancer.

| S-EPMC6134008 | biostudies-literature

GATA1-deficient dendritic cells display impaired CCL21-dependent migration towards lymph nodes due to reduced levels of polysialic acid

Project description:Dendritic cells (DCs) play a pivotal role in the regulation of the immune response. DC development and activation is finely orchestrated through transcriptional programs. GATA1 transcription factor is required for murine DC development and data suggests that it might be involved in the fine-tuning of the life span and function of activated DCs. We generated DC-specific Gata1 knockout mice (Gata1-KODC), which presented a 20% reduction of splenic DCs, partially explained by enhanced apoptosis. RNA-Seq analysis revealed a number of deregulated genes involved in cell survival, migration and function. DC migration towards peripheral lymph nodes was impaired in Gata1-KODC mice. Migration assays performed in vitro showed that this defect was selective for CCL21, but not CCL19. Interestingly, we show that Gata1-KODC DCs have reduced polysialic acid levels on their surface, which is a known determinant for the proper migration of DCs towards CCL21.

2016-11-08 | GSE69969 | GEO

LACTIPLANTIBACILLUS PLANTARUM STRENGTHENS THE INTESTINAL BARRIER: INVOLVEMENT OF THE ENDOCANNABINOIDOME

Project description:LACTIPLANTIBACILLUS PLANTARUM STRENGTHENS THE INTESTINAL BARRIER: INVOLVEMENT OF THE ENDOCANNABINOIDOME

| PRJNA1098776 | ENA

CCL21/CCR7 axis in regulating glioblastoma stem cell-lymphatic endothelial cell interaction

Project description:CCL21/CCR7 axis in regulating glioblastoma stem cell-lymphatic endothelial cell interaction

| PRJNA901970 | ENA

Characteristics of a CCL21-gene modified dendritic cell vaccine utilized for a clinical trial in non-small cell lung cancer

Project description:Samples are from a phase I clinical trial of a vaccine consisting of monocyte-derived DCs (moDCs) modified to express the chemokine CCL21 given in combination with pembrolizumab, conducted in patients with advanced non-small cell lung cancer. Single cell RNA sequencing of pre- and post-transduced vaccines was performed to characterize the cellular composition of these vaccines and assess the trascriptional impact of the transduction process. The same vaccine production procedure was also applied to blood obtained from healthy donors to investigate the effects of donor source on DC vaccine phenotype.

2024-11-14 | GSE272174 | GEO

Dual mTOR/PI3K inhibition limits PI3K-dependent pathways activated upon mTOR inhibition in autosomal dominant polycystic kidney disease.

Project description:Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the development of kidney cysts leading to kidney failure in adulthood. Inhibition of mammalian target of rapamycin (mTOR) slows polycystic kidney disease (PKD) progression in animal models, but randomized controlled trials failed to prove efficacy of mTOR inhibitor treatment. Here, we demonstrate that treatment with mTOR inhibitors result in the removal of negative feedback loops and up-regulates pro-proliferative phosphatidylinositol 3-kinase (PI3K)-Akt and PI3K-extracellular signal-regulated kinase (ERK) signaling in rat and mouse PKD models. Dual mTOR/PI3K inhibition with NVP-BEZ235 abrogated these pro-proliferative signals and normalized kidney morphology and function by blocking proliferation and fibrosis. Our findings suggest that multi-target PI3K/mTOR inhibition may represent a potential treatment for ADPKD.

| S-EPMC5882886 | biostudies-other

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