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Glucocorticoids and the cytokines IL-12, IL-15 and IL-18 present in the tumor microenvironment induce PD-1 expression on human Natural Killer cells

ABSTRACT: Glucocorticoids and the cytokines IL-12, IL-15 and IL-18 present in the tumor microenvironment induce PD-1 expression on human Natural Killer cells

PROVIDER: PRJNA627411 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11588746_1.fastq.gz	Fastqsanger.gz
	SRR11588746_2.fastq.gz	Fastqsanger.gz
	SRR11588747_1.fastq.gz	Fastqsanger.gz
	SRR11588747_2.fastq.gz	Fastqsanger.gz
	SRR11588748_1.fastq.gz	Fastqsanger.gz

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Glucocorticoids and the cytokines IL-12, IL-15 and IL-18 present in the tumor microenvironment induce PD-1 expression on human Natural Killer cells

Project description:Background: PD-1 immune checkpoint blockade has provided significant clinical efficacy across various types of cancer by unleashing both T- and NK cell-mediated anti-tumor responses. However, resistance to immunotherapy occurs for many patients, rendering the identification of the mechanisms that control PD-1 expression extremely important to increase the response to the therapy Objective: To identify the stimuli and the molecular mechanisms that induce the de novo PD-1 expression on human NK cells in the tumor setting Methods: NK cells freshly isolated from peripheral blood of healthy donors were stimulated with different combinations of molecules, and PD-1 expression was studied at the mRNA and protein level. Moreover, ex vivo analysis of tumor microenvironment and NK cell phenotype was performed. Results: Glucocorticoids (GCs) are indispensable for PD-1 induction on human NK cells, in cooperation with a combination of cytokines that are abundant at the tumor site. Mechanistically, GCs together with IL-12, IL-15 and IL-18 not only upregulate PDCD1 transcription, but also activate a previously unrecognized transcriptional program leading to enhanced mRNA translation and resulting in an increased PD-1 protein amount in NK cells. Conclusion: Our results provide evidence of a novel immune suppressive mechanism of GCs involving the transcriptional and translational control of an important immune checkpoint

2020-04-23 | GSE149113 | GEO

Transcriptional changes in IL-2, IL-12 and IL-18 stimulated human natural killer cells

Project description:We used Affymetrix expression arrays to determine changes in gene expression associated with activation of human NK cells mediated through treatment with cytokines IL-2, IL-12 and IL-18 over a 24 hour period. Human natural killer cells were isolated via negative selection from PBMCs of healthy donors. Cells were found to be > 95% CD3-CD56+. RNA was harvested at time of isolation or after 24 hour stimulation from 8 x 10^6 cells per condition. For stimulations, cells were incubated at 37C (5% CO2) in RPMI, suuplemented with 10% Fetal Bovine Serum at 1.5 x 10^6 cells/ml. Cytokine stimualtions were conducted with IL-2 (100U/mL), IL-12 (10ng/mL) and IL-18 (100ng/mL) from 2 male donors (N = 4). Expression analysis was carried out to determine transcriptional changes associated with 24 hr stimulation relative to freshly isolated cells.

2010-08-05 | E-GEOD-22919 | biostudies-arrayexpress

Protein phosphorylations, mediated by pro-inflammatory cytokines IL-32g and IL-17A/F

Project description:Global kinase activity induced by cytokines IL-32g and IL-17A/F were determined using peptide arrays representing phophorylation targets The objective of this study was to identify common and unique phosphorylation targets of pro-inflammatory cytokines IL-32 and IL-17. These cytokines are associated with the pathogenesis and severity of chronic inflammatory disorders, therefore signaling intermediates of these cytokines could be beneficial as alternate theraputic targets that may likely influence different inflammatory pathways. Phosphorylation of proteins is a critical mechanism in the regulation of cellular processes. This process is meticulously regulated by enzymes known as kinases, which are increasingly being identified as drug targets for a variety of diseases. In this study we interrogated kinase activities (kinome) induced in the presence of the human recombinant cytokines IL-32g and IL-17A/F employing peptide arrays representing 300 peptides, printed in triplicate, representing select phosphorylation events. Human macrophage-like THP-1 cells were used for this comparative kinome analysis. Macrophage-like THP-1 cells were stimulated with either IL-32g (20 ng/ml) or IL-17A/F (20 ng/ml) for 15 min, and the peptide arrays were used to comprehensively analyze protein phosphorylation profiles in the presence of these cytokines. Two independet biological experiments were performed and the kinoem analysis was done in triplicates for each. The phosphorylations of the peptides on the array were quantified in the cytokine-treated cells relative to the un-stimulated control cells. Differentially phosphorylated targets were defined as greater than 1.5 fold increase or decrease (p < 0.06) in phosphorylation compared to un-stimulated control cells.

2011-04-16 | E-GEOD-28649 | biostudies-arrayexpress

Protein phosphorylations, mediated by pro-inflammatory cytokines IL-32g and IL-17A/F

2011-04-16 | GSE28649 | GEO

Proteomic analysis of human eosinophils stimulated with IL-4 and IL-5

Project description:Activated eosinophils is a major cell type to be involved in allergic diseases. Type 2 cytokines (IL-4 and IL-5) are important to establish and augment their inflammatory process. The aim of this study is to clarify the role of these cytokines as direct activators for human eosinophils.

2024-06-20 | PXD052200 | JPOST Repository

Multiple IL-17 family cytokines signaling through IL-17RA drive inflammatory pathways in psoriasis

Project description:The IL-23/IL-17 immune axis is of central importance in psoriasis. However, the contribution of IL-17 family cytokines other than IL-17A to drive skin inflammation in psoriasis has not been fully established. To further elucidate the role of individual IL-17 family cytokines in psoriasis, we investigated their expression and localization in psoriasis skin at the mRNA and protein level. Moreover, we investigated the gene expression signatures induced by individual IL-17 family cytokines in human skin ex vivo as well as modulation of responses induced by the combination of IL-17 family cytokines in human keratinocytes by brodalumab, a human monoclonal antibody targeting the IL-17RA, versus the IL-17A blocking antibody ixekizumab. We demonstrate that IL-17A, IL-17AF, IL-17F and IL-17C are expressed at increased levels in psoriasis lesional skin and induce inflammatory gene expression signatures in human skin ex vivo that correlate with those observed in psoriasis. Furthermore, we show that brodalumab, in contrast to ixekizumab, fully blocks gene expression responses induced by the combination of IL-17A, IL-17AF, IL-17F and IL-17C in human keratinocytes. These findings suggest that inhibition of several IL-17 family cytokines, e.g. by targeting of the IL-17RA receptor, could be a favored mechanism to obtain a profound suppression of the inflammatory processes in psoriasis and thereby achieve high levels of skin clearance and sustained efficacy in patients with psoriasis.

2021-04-07 | GSE158448 | GEO

Reconstituted human epidermis cultures treated with IL-1 family cytokines for 24 hours.

Project description:Analysis of stratified epidermal cultures treated with IL-1a, IL-1F5, IL-1F6, IL-1F8 and IL-1F9 to determine the effects of these cytokines at 24h. Results provide insight into the role of IL-1 family cytokines in the pathogenesis of psoriasis. 16 samples. 2 untreated controls, 14 cytokine treated

2010-11-17 | E-GEOD-25400 | biostudies-arrayexpress

Reconstituted human epidermis cultures treated with IL-1 family cytokines for 24 hours.

2010-11-17 | GSE25400 | GEO

Transcriptional changes in IL-2, IL-12 and IL-18 stimulated human natural killer cells

2010-08-05 | GSE22919 | GEO

Human islets exposed to cytokines IL-1β and IFN-γ

Project description:In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death. Human islets were isolated and exposed (or not) to IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix arrays. These measurements were performed three times.

2013-12-19 | E-GEOD-53454 | biostudies-arrayexpress

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