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Qualitatively Different T Cell Phenotypic Responses to IL-2 versus IL-15 are Unified by Identical Dependences on Receptor Signal Strength and Duration

ABSTRACT: 3 biological replicates of F15R-Kit cells stimulated with 500pM IL-2 or IL-15 for 15 minutes, and two biological replicates of unstimulated cells (total 8 conditions) were iTRAQ8plex labeled, combined and analyzed together. Phosphotyrosine peptides were enriched for by immunoprecipitation followed by further enrichment by IMAC. Peptides were anaylzed on an Orbitrap Elite with CID and HCD scans for MS/MS peptide identification.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): T Cell, Blood

SUBMITTER: Hannah Johnson

LAB HEAD: Hannah Johnson

PROVIDER: PXD000440 | Pride | 2013-11-07

REPOSITORIES: Pride

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			Action	DRS
	HJ110112_IL2and15_E.raw	Raw
	PRIDE_Exp_Complete_Ac_31010.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_31010.pride.mztab.gz	Mztab
	PRIDE_Exp_Complete_Ac_31010.xml.gz	Xml

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Publications

Qualitatively different T cell phenotypic responses to IL-2 versus IL-15 are unified by identical dependences on receptor signal strength and duration.

Arneja Abhinav A Johnson Hannah H Gabrovsek Laura L Lauffenburger Douglas A DA White Forest M FM

Journal of immunology (Baltimore, Md. : 1950) 20131202 1

IL-2 and IL-15 are common γ-chain family cytokines involved in regulation of T cell differentiation and homeostasis. Despite signaling through the same receptors, IL-2 and IL-15 have non-redundant roles in T cell biology, both physiologically and at the cellular level. The mechanisms by which IL-2 and IL-15 trigger distinct phenotypes in T cells remain elusive. To elucidate these mechanisms, we performed a quantitative comparison of the phosphotyrosine signaling network and resulting phenotypes ...[more]

PMID: 24298013

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Dissection of IL-2 and IL-15 signaling pathways

Project description:The aim of this study was to compare the signaling cascades initiated by the two closely related cytokines IL-2 and IL-15. Considering the relevance of protein tyrosine phosphorylation in signal transduction, in order to quantify changes in protein phosphorylation in response to IL-2 and IL-15, we combined triple SILAClabeling of leukemic T-cells with phosphotyrosine (pY)-specific antibody-based protein enrichment followed by mass spectrometry (MS) analysis. Following the strategy described above, we managed to decipher in detail the complex signaling networks triggered by IL-2 and IL-15. Interestingly, a large number of components of the three main signaling pathways known to be initiated in response to the interleukins (JAK/STAT; RAS/MAPK; PI3K/AKT) were identified.

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Activation of Sez-4 cell line with IL-2, IL-15 or IL-21.

Project description:In this study we compared the effects of IL-2, IL-15, and IL-21 on the gene expression, activation of cell signaling pathways, and functional properties of cells derived from the CD4+ cutaneous T-cell lymphoma (CTCL). Whereas both IL-2 and IL-15 that signal through receptors that share the common gamma chain and the beta chain modulated the expression of >1,000 genes, IL-21 that signals via the receptor also containing gamma chain up-regulated <40 genes. All three cytokines induced tyrosine phosphorylation of Jak1 and Jak3. However, only IL-2 and IL-15 strongly activated STAT5, PI3K/Akt, and MEK/ERK signaling pathways. In contrast, IL-21 selectively activated STAT3. Whereas all three cytokines protected CTCL cells from apoptosis, only IL-2 and IL-15 promoted their proliferation. The effects of the cytokine stimulation were Jak3- and Jak1-kinase dependent. These findings document the vastly different impact of IL-2 and IL-15 vs. IL-21 on malignant CD4+ T cells. They also suggest two novel therapeutic approaches to CTCL and, possibly, other CD4+ T cell lymphomas: inhibition of the Jak1/Jak3 kinase complex and, given the known strong immunostimulatory properties of IL-21 on CD8+ T, NK, and B cells, application of this cytokine to boost an immune response against malignant CD4+ T cells. Keywords: 3 replicates in each of 4 conditions

2008-02-19 | GSE8685 | GEO

RNA Expression Data from IL-15-/- and IL-15+/+ TAX-LUC Mouse Tumors

Project description:IL-15 is recognized as a promising candidate for tumor immunotherapy and has been described as both a promoter of cancer and a promoter of anti-cancer immunity. IL-15 was discovered in cells transformed by HTLV-1, the etiologic agent of adult T cell leukemia / lymphoma (ATL) and the human retrovirus that carries the Tax oncogene. We have developed the TAX-LUC mouse model of ATL in which Tax expression drives both malignant transformation and luciferase expression, enabling non-invasive imaging of tumorigenesis in real time. To identify the role of IL-15 in spontaneous development of lymphoma in vivo, an IL-15-/- TAX-LUC strain was developed and examined. The absence of IL-15 resulted in aggressive tumor growth and accelerated mortality and demonstrated that IL-15 was not required for Tax-mediated lymphoma but was essential for anti-tumor immunity. Further analysis revealed a unique transcriptional profile in tumor cells that arise in the absence of IL-15 that included a significant increase in the expression of IL-1α and IL-1α-regulated cytokines. Moreover, anti-IL-1α antibodies and an IL-1 receptor antagonist (Anakinra) were used to interrogate the potential of IL-1α targeted therapies in this model. Taken together, these findings identify IL-15 and IL-1α as therapeutic targets in lymphoma. We used microarrays to compare the gene expression profile of tumors in IL-15-/- TAX-LUC mice to IL-15+/+ TAX-LUC mice

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Qualitatively different T cell phenotypic responses to IL-2 versus IL-15 are unified by identical dependences on receptor signal strength and duration.

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Effect of IL-15 culture +/- anti-NK1.1 stimulation on splenic NK cells [mNK_IL-15_RNA-seq]

Project description:Splenic NK cells were enriched and cultured in either low dose (5-10 ng/ml) or high dose (100 ng/ml) IL-15. Naïve NKs are freshly enriched NKs, obtained the day of the anti-NK1.1 stimulation. Cells were either left unstimulated or were stimulated via plate-bound anti-NK1.1

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RNA Expression Data from IL-15-/- and IL-15+/+ TAX-LUC Mouse Tumors

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Comprehensive proteomics analyses of IL-15 driven activation of intestinal intraepithelial lymphocytes

Project description:Intestinal intraepithelial lymphocytes (IEL) are an abundant population of tissue-resident T cells that protect the gut from pathogens and maintain intestinal homeostasis. The cytokine IL-15 is trans-presented by epithelial cells to IEL in complex with the IL-15 receptor α chain (IL-15Rα) and plays essential roles both in maintaining IEL homeostasis, and in inducing IEL activation in response to epithelial stress. When overproduced, IL-15 is a key driver of the gluten-induced enteropathy Coeliac disease, through cytotoxic activation of IEL. To better understand how IL-15 directly regulates both homeostatic and inflammatory functions of IEL, we performed quantitative proteomics of IL-15/Rα-stimulated murine IEL, sorted into their 3 main subpopulations, TCRγδ CD8αα, TCRαβ CD8αβ and TCRαβ CD8αα expressing IEL. The data reveal that high IL-15/Rα stimulation licenses cell cycle activation, upregulates the biosynthetic machinery in IEL, increases mitochondrial respiratory capacity and induces expression of cell surface immune receptors and adhesion proteins that potentially drive IEL activation.

2021-05-10 | PXD025891 | Pride

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Project description:We isolated splenic NK cells and cultured them for 3 days in 100 ng/ml IL-15. Next, we stimulated the cells with plate-bound anti-NK1.1 for 6 hours and sorted YFP+ (IFNg+) and YFP- (IFNg-) populations. We then performed gene expression profiling analysis using data obtained from RNA-seq from unstimulated, YFP+ or YFP- NK cells.

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