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Transcriptomic response to ex vivo IL33 stimulation of blood eosinophils from mepolizumab- or omalizumab-treated patients

ABSTRACT: Transcriptomic response to ex vivo IL33 stimulation of blood eosinophils from mepolizumab- or omalizumab-treated patients

PROVIDER: PRJEB43462 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5418270_1.fastq.gz	Fastqsanger.gz
	ERR5418270_2.fastq.gz	Fastqsanger.gz
	ERR5418261_1.fastq.gz	Fastqsanger.gz
	ERR5418261_2.fastq.gz	Fastqsanger.gz
	ERR5418271_1.fastq.gz	Fastqsanger.gz

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Transcriptomic response to ex vivo IL33 stimulation of blood eosinophils from mepolizumab- or omalizumab-treated patients

Project description:Coding RNA expression of blood eosinophils from mepolizumab- or omalizumab-treated patients stimulated ex vivo with IL-33 for 6 hours and of directly processed non-stimulated blood eosinophils from the same samples (paired design)

2021-12-17 | E-MTAB-10189 | biostudies-arrayexpress

Comparison of coding RNA expression of blood eosinophils from mepolizumab- or omalizumab-treated severe asthmatic patients and from healthy controls

Project description:RNA-seq comparison of coding RNA expression in blood eosinophils from patients with severe allergic eosinophilic asthma treated with mepolizumab with those of healthy controls and matched severe asthmatic patients receiving omalizumab.

2021-12-17 | E-MTAB-10190 | biostudies-arrayexpress

Expression data from study on IL33 signaling in Dusp5 deficient eosinophils

2014-11-06 | GSE62999 | GEO

Comparison of coding RNA expression in steady-state and in response to IL33 and IL5 stimulation in bone marrow eosinophils from IL5-deficient and wild-type littermates

Project description:Aim of the experiment was to assess differences in expression of coding RNA between bone marrow eosinophils arising in IL-5 knock-out mice (C57BL/6-Il5tm1Kopf/J) or wild-type littermates and their response to cytokine stimulation. Bone marrow eosinophils were sorted by FACS submitted to RNA-seq immediately or after 4 hours of stimulation with IL-5 and IL-33 in culture plates.

2021-12-17 | E-MTAB-10188 | biostudies-arrayexpress

Henderson omalizumab study

Project description:A considerable proportion of patients with H1-antihistamine-resistant chronic spontaneous urticaria (CSU) fails to respond to omalizumab. However, there is yet no available biomarker that accurately predicts such a response outcome. The utility of blood basophil and eosinophil levels and exosomal and basophil micro(mi)RNAs as biomarkers of response to omalizumab in CSU was explored. In this prospective cohort study of twenty patients with antihistamine-resistant CSU, subjects were treated with 3-monthly doses of omalizumab, and their response assessed using the weekly urticaria activity score (UAS7) for a period of 12-weeks. Basophil and eosinophil levels in the blood and differentially expressed exosomal and basophil miRNAs of complete responders compared to non-responders were identified at baseline. Canonical pathways, altered by differentially expressed miRNAs, were identified using Ingenuity Pathway Analysis (IPA). Complete responders had higher baseline basophil levels (≥21 cells/L) in the peripheral blood compared to non-responders (P = 0.005). Baseline levels of eosinophils did not differ between the study groups. Complete responders in comparison to non-responders had an expression profile characterized by a significantly higher expression of six exosomal miRNAs (miR-6499-5p, miR-7848, miR-4494-3p, miR-450a-2-3p, miR-6877-3p, and miR-3976) and lower expression of miR-141-3p. Complete responders also had higher expression of three basophil miRNAs (miR-1200, miR-1236-3p, and miR-4496). The exosomal miRNA expression profile was predicted by IPA to alter Tec Kinase Signaling pathway activity (P = 0.003).

2021-11-16 | GSE153579 | GEO

Expression data from study on IL33 signaling in Dusp5 deficient eosinophils

Project description:Dusp5 regulates ERK phosporylation following IL-33 receptor ligation in cultured eosinophils. Dusp5 deficient eosinophils show increased ERK phosphorylation, and as a result are less apoptotic. Since ERK stimulation results in downstream activation of transcription factors, we are utilizing a microarray approach to find alterations in gene expression to uncover potential mechanisms for increased cell survival. Day 12 bone marrow derived eosinophils from Dusp5+/+ and Dusp5-/- mice (5 mice per genotype) were left untreated (media only) or IL-33 (25ng/ml) stimulated for 4 hours. Treated cells were washed with ice cold PBS and cell pellets were directly lysed in RLT buffer (Qiagen) followed by immediate RNA isolation (RNEasy plus mini kit with genomic DNA eliminator columns). Sample group names: Group 1- Dusp5+/+ Untreated (N=5) Group 2- Dusp5-/- Untreated (N=5) Group 3- Dusp5+/+ IL-33 4hrs (N=5) Group 4- Dusp5-/- IL-33 4hrs (N=5) Sample Names: Group 1- BM Eos unstimulated WT-1....WT-5 Group 2- BM Eos unstimulated Dusp5-/- -1......Dusp5-/- -5 Group 3- BM Eos IL-33 4hrs WT-1....WT-5 Group 4- BM Eos IL-33 4hrs Dusp5-/- -1......Dusp5-/- -5

2014-11-06 | E-GEOD-62999 | biostudies-arrayexpress

Henderson omalizumab study

Project description:Henderson omalizumab study

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Whole blood transcriptional variations between responders and non-responders in asthma patients receiving omalizumab

Project description:To investigate blood transcriptional changes induced by omalizumab treatment and to determine variations between omalizumab responders and non-responders.

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Gene expression profiling of small intestinal eosinophils of BALB/c mice after stimulation with GM-CSF

Project description:Next generation sequencing was performed to conprehensively investigate the changes of gene expression of small intestinal eosinophils of mice after stimulation with GM-CSF in vitro.

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Proteomic analysis of IL33-proximal proteins in squamous cell carcinoma cells

Project description:Focal adhesion kinase (FAK) is required for the expression of pro-inflammatory genes that inhibit anti-tumour immunity. Here, we show a novel and crucial role for the dual-function cytokine IL33 in FAK-dependent immune evasion. Specifically, nuclear FAK is required for the expression of IL33, the chemokine Ccl5 and the soluble form of the IL33 receptor, sST2, which are required for evasion of CD8+ T-cell-mediated anti-tumour immunity. Mechanistically, nuclear IL33 associates with FAK and a network of chromatin modifiers and transcriptional regulators, including Taf9, WDR82 and BRD4, while sST2 likely negates effects of IL33 secreted into the tumour microenvironment by infiltrating host immune cells. Finally, protein interaction network analysis implies that nuclear FAK–IL33 complexes impact on transcription factors that regulate NFkB and chemokines like Ccl5 downstream. Our data therefore provide new mechanistic insight into how FAK controls the tumour immune environment via a FAK–IL33/sST2 pathway and demonstrate a novel role for nuclear IL33 downstream of FAK as a component of transcription regulatory complexes that critically modulate anti-tumour immunity.

2017-12-06 | PXD007698 | Pride

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