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TGF-b1 stimulates lymphatic endothelial cells to produce IL-7 and IL-15, which act as chemotactic factors for breast cancer cells with EMT properties

ABSTRACT: TGF-b1 stimulates lymphatic endothelial cells to produce IL-7 and IL-15, which act as chemotactic factors for breast cancer cells with EMT properties

PROVIDER: PRJNA1010671 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25786839.fastq.gz	Fastqsanger.gz
	SRR25786840.fastq.gz	Fastqsanger.gz
	SRR25786841.fastq.gz	Fastqsanger.gz
	SRR25786842.fastq.gz	Fastqsanger.gz
	SRR25786843.fastq.gz	Fastqsanger.gz

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TGF-b1 stimulates lymphatic endothelial cells to produce IL-7 and IL-15, which act as chemotactic factors for breast cancer cells with EMT properties

Project description:The lymphatic system is a major gateway for tumor cell dissemination but the mechanisms of how tumor cells gain access to lymphatic vessels are not completely understood. Breast cancer cells undergoing epithelial-mesenchymal transition (EMT) gain invasive and migratory properties. Overexpression of the cytokine transforming growth factor β1 (TGF-b1), a potent inducer of EMT, is frequently detected in the tumor microenvironment and correlates with invasion and lymph metastasis. Recently, we reported that TGF-b1 stimulated breast cancer cells with EMT properties migrate in a targeted fashion towards the lymphatic system via CCR7/CCL21-mediated chemotaxis, similar to dendritic cells during inflammation. Here, we aimed to identify additional chemotactic factors and receptors that could be involved in this. Through a combination of RNA sequencing analysis, database screening and invasion assays we identified IL-7/IL7R and IL-15/IL15R as pairs of chemokines and chemokine receptors with potential roles in promoting chemotactic migration of breast cancer cells with EMT properties towards the lymphatics. The results warrant studies to further explore their possible roles in lymph metastasis in breast cancer. Moreover, they demonstrate the capacity of TGF-b1 to orchestrate crosstalk between tumor cells and lymphatic endothelial cells.

2023-12-13 | GSE241881 | GEO

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IL-17 cytokines preferentially act on naïve CD4+ T cells

Project description:CD4+ Th17 T cells are a key helper population in the regulation of both protective immunity during infection and in self-tolerance. Through the secretion of IL-17, Th17 cells act in promotion of inflammation and thus a major therapeutic target for autoimmune disorders. Recent reports have brought to light that the IL-17 family cytokines, IL-17A, IL-17F and IL-17AF, can directly act on CD4+ T-cells, both in murine and human systems. Here we show that this action is preferentially targeted toward naïve, but not memory, CD4+ T-cells. Moreover, IL-17A, IL-17F and IL-17AF led to reduction in immune signaling genes, but an increase in interferon responsive genes across all treatments. In addition, IL-17A, IL-17F and IL-17AF treatment possessed differences in downstream transcriptional signaling, with IL-17AF heterodimer conferring both the greatest transcriptional change and suppressed phenotype. Detailed transcriptome analysis provides important functional insights into the genes and pathways that are modulated as a result of IL-17-mediated signaling.

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TGFß1 Stimulates Lymphatic Endothelial Cells to Produce IL7 and IL15, Which Act as Chemotactic Factors for Breast Cancer Cells with Mesenchymal Properties.

Project description:The lymphatic system is a major gateway for tumor cell dissemination but the mechanisms of how tumor cells gain access to lymphatic vessels are not completely understood. Breast cancer cells undergoing epithelial-mesenchymal transition (EMT) gain invasive and migratory properties. Overexpression of the cytokine transforming growth factor β1 (TGFβ1), a potent inducer of EMT, is frequently detected in the tumor microenvironment and correlates with invasion and lymph metastasis. Recently, we reported that TGFβ1 stimulated breast cancer cells with mesenchymal properties to migrate in a targeted fashion towards the lymphatic system via CCR7/CCL21-mediated chemotaxis, similar to dendritic cells during inflammation. Here, we aimed to identify additional chemotactic factors and corresponding receptors that could be involved in guiding breast cancer cells through the lymphatic system. Through a combination of RNA sequencing analysis, database screening and invasion assays we identified IL7/IL7R and IL15/IL15R as pairs of chemokines and receptors with potential roles in promoting chemotactic migration of breast cancer cells with mesenchymal properties towards the lymphatics. The results demonstrate the capacity of TGFβ1 to orchestrate crosstalk between tumor cells and lymphatic endothelial cells and warrant further studies to explore the roles of IL7 and IL15 in promoting lymph metastasis of breast cancer.

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IL-17 cytokines preferentially act on naïve CD4+ T cells

Project description:IL-17 cytokines preferentially act on naïve CD4+ T cells

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IL-6R identifies early differentiated human effector memory CD8+ T cells that potently expand and produce IL-2 and IL-13

Project description:We found a unique subset of effector memory (EM) CD8+ T cells that expressed high levels of IL-6 receptor in human peripheral blood. These cells which also expressed high levels of IL-7Ra (referred to as IL-6R high IL-7Rahigh cells) had the a distinct gene expression profile and cellular characteristics compared to other EM CD8+ T cells. IL-6R high IL-7Ra high cells were early differentiated EM CD8+ T cells with decreased expression of T-bet, KLRG1, perforin and granzyme B. These cells had increased cell proliferation likely secondary to enhanced IL-2 production and high affinity IL-2R expression. IL-6R high IL-7Ra high EM CD8+ T cells exclusively produced high levels of IL-2, IL-5, IL-9 and IL-13 although IFN-r was produced by this cell subset and other EM CD8+ T cells. Of interest, IL-6R high IL-7Ra high EM CD8+ T cells expanded in the peripheral blood of patients with chronic obstructive pulmonary disease (COPD) and asthma where CD8+ T cells, IL-13 and IFN-r are suggested to be involved in the pathogenesis. Being the early-differentiated EM CD8+ T cells with a potent capacity to proliferate, survive and generate multiple cytokines, IL-6R high IL-7Ra high EM CD8+ T cells may serve as a primary reservoir for effector CD8+ T cells which potently expand and produce cytokines upon immune stimulation. Duplicate experiments were performed for each condition. In each condition, we independently prepared total RNA using the RNeasy mini kit (Qiagen) and assessed RNA integrity using Bioanalyzer 2100 (Agilent)- RINs were close to 10 for all samples. RNA was then amplified and hybridized to the Illumina HumanHT-12 v4.0 BeadChip, according to Illumina standard protocols.

2012-12-31 | E-GEOD-34562 | biostudies-arrayexpress

IL-6R identifies early differentiated human effector memory CD8+ T cells that potently expand and produce IL-2 and IL-13

2012-12-31 | GSE34562 | GEO

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Myeloid cell-derived proteases produce a proinflammatory form of IL-37 that signals via IL-36 receptor engagement

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FIP-fve stimulates cell proliferation and enhances IL-2 release by activating MAP2K3/p38α（MAPK14）signaling pathway in Jurkat E6-1 cells

Project description:FIP-fve, a fungal fruiting body protein from Flammulina velutipes, has potential immunomodulatory properties. Here, we investigated the immunomodulation mechanism of FIP-fve in Jurkat E6-1 cells by conducting cell viability assay and IL-2 release assay. Kinase inhibitors experiment and proteomics analysis were also involved in the mechanism study. It was found that FIP-fve stimulated cell proliferation and enhanced IL-2 secretion in a dose-dependent manner in Jurkat E6-1 cells. Unbiased high-throughput proteomics analysis showed that 4 T cell immune activation markers including ZAP-70, CD69, CD82 and KIF23 were upregulated in response to FIP-fve treatment. Further pathway analysis indicated that MAP2K3/p38 pathway related proteins including MAP2K, p38, ELK, AATF, FOS, and JUN-B were unregulated. In addition, losmapimod (p38 inhibitor) and gossypetin (MAP2K3 inhibitor) inhibited FIP-fve enhanced cell proliferation and IL-2 release in Jurkat E6-1 cells. Our results demonstrate that FIP-fve stimulates cell proliferation and enhances IL-2 secretion through MAP2K3/ p38α activation.

2022-06-09 | PXD032302 | Pride

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