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Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

ABSTRACT: Gene expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. Patient CLL01 was also treated with IL-4 plus 5 mg/ml ERK activation inhibitor peptide I, or IL-4 plus 10 ÂµM NFkB activation inhibitor, and IL-4 plus 100 mg/ml cyclic-pifithrin-Î± 23 CLL patients (10 Pre samples, 23 Ctrl samples, 23 IL-4 samples, 1 IL-4 plus ERK inhibitor sample, 1 IL-4 plus NFkB inhibitor sample, 1 IL-4 plus Pifithrin sample), 13 NBC (10 Pre samples, 10 Ctrl samples, 13 IL-4 samples)

ORGANISM(S): Homo sapiens

SUBMITTER: Antonio Parrado

PROVIDER: E-GEOD-55288 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The gene expression response of chronic lymphocytic leukemia cells to IL-4 is specific, depends on ZAP-70 status and is differentially affected by an NFκB inhibitor.

Ruiz-Lafuente Natalia N Alcaraz-García María-José MJ Sebastián-Ruiz Silvia S Gómez-Espuch Joaquín J Funes Consuelo C Moraleda José-María JM García-Garay María-Carmen MC Montes-Barqueros Natividad N Minguela Alfredo A Álvarez-López María-Rocío MR Parrado Antonio A

PloS one 20141003 10

Interleukin 4 (IL-4), an essential mediator of B cell development, plays a role in survival of chronic lymphocytic leukemia (CLL) cells. To obtain new insights into the function of the IL-4 pathway in CLL, we analyzed the gene expression response to IL-4 in CLL and in normal B cells (NBC) by oligonucleotide microarrays, resulting in the identification of 232 non-redundant entities in CLL and 146 in NBC (95 common, 283 altogether), of which 189 were well-defined genes in CLL and 123 in NBC (83 co ...[more]

PMID: 25280001

Similar Datasets

Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

Project description:Gene expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. Patient CLL01 was also treated with IL-4 plus 5 mg/ml ERK activation inhibitor peptide I, or IL-4 plus 10 µM NFkB activation inhibitor, and IL-4 plus 100 mg/ml cyclic-pifithrin-α

2014-10-06 | GSE55288 | GEO

miRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

Project description:miRNA expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. 16 CLL patients (8 Pre samples, 15 Ctrl samples, 15 IL-4 samples), 3 NBC (3 Ctrl samples, 3 IL-4 samples)

2015-06-15 | E-GEOD-62137 | biostudies-arrayexpress

miRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

Project description:miRNA expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples.

2015-06-15 | GSE62137 | GEO

Recombinant IL-1 RA in human Chronic lymphocytic leukemia cells in vitro

2023-10-04 | GSE236552 | GEO

A phase I trial of the IL1-receptor antagonist anakinra in previously untreated CLL patients at risk for progression

Project description:Inflammatory factors that activate NFkB play an important role in the pathogenesis of chronic lymphocytic leukemia (CLL) but are not addressed specifically by current therapies. Interleukin-1 (IL-1) is a master-regulator of inflammation that is inhibited safely in humans by the IL-1 receptor antagonist anakinra. Anakinra was found to inhibit NFkB activity in CLL cells in an IL-1 receptor independent manner and had properties of an intracellular anti-oxidant in vitro. A phase I dose-escalation trial in 11 previously untreated CLL patients (NCT04691765) indicated anakinra was safe at doses up to 400 mg daily and produced transient clinical responses associated with down-regulation of NFkB and oxidative stress in circulating CLL cells in vivo. However, type 1 interferon (IFN)-signaling and c-MYC-regulated genes and proteins were induced at the same time.

2023-10-04 | GSE236606 | GEO

RNA-seq analysis of GCBC and NBC that had been stimulated for either 2h or 4h with IL-21, CD40 ligation, BCR ligation, or combinations of these.

Project description:Purpose: To gain insight into both similarities and differences in the gene expression programs induced by IL-21R, BCR and CD40 signals, we performed RNA-seq on both GCBC and NBC that had been stimulated for either 2h or 4h with IL-21, CD40 ligation, BCR ligation, or combinations of these. Methods : Purified GCBC from d14 NP-CGG immunized MEG mice and NBC from naïve MEG mice were warmed at 37C for 30 minutes and then stimulated with 10ng/mL IL-21, 20μg/ml ⍺-IgM or 2.5μg/mL ⍺-CD40 (prepared as tetramer) alone or combined IL21/⍺-CD40 or ⍺-IgM/⍺-CD40 for 2 and 4 hours. After stimulation, cells were processed for RNA isolation using QIAshredder columns (Qiagen) and the RNeasy Plus Mini Kit (Qiagen) following the manufacturer’s instructions. Samples were sequenced using Illumina NextSeq 500 with 75 bp paired-end reads and aligned to the mm10 genome using the STAR aligner (Dobin et al., 2013). Gene-level counts were determined using featureCounts (Liao et al., 2014), and raw counts were quantile normalized to each other for differential expression using the voom method (Law et al., 2014) in the Limma R package (Ritchie et al., 2015). For normalization of the datasets, the Quantile method was used. Results: Like BCR and CD40 signals, IL-21R plus CD40 signals also synergize to induce c-Myc in GCBC. However, IL-21R plus CD40 stimulation differentially affects GCBC fate compared to BCR plus CD40 ligation—engaging unique molecular mechanisms

2023-02-16 | GSE197662 | GEO

Homo sapiens

Project description:Gamma-secretase inhibitor plus fludarabine in CLL

| PRJNA219743 | ENA

Assessment of the impact of the IL23R R381Q variant in terms of IL-23-sensitive transcript induction

Project description:We stimulated T-cell blasts from IL23R R381Q homozygotes (n = 2), healthy controls homozygous for the ancestral allele (n = 9), homozygous individuals for TYK2 P1104A (n = 2) that selectively impairs responses to IL-23, and one patient each with autosomal recessive, complete TYK2 or IL-12Rb1 deficiency with IL-12, IL-23, IL-1b, and IL-1b plus IL-23 for 6 hours and performed RNA-sequencing. We used IL-1b as an IL-23-sensitizing agent as previously reported. We found that while T-cell blasts from IL23R R381Q homozygotes respond normally to IL-12 and IL-1b, their response to IL-23 and to IL-23 plus IL-1b is impaired

2023-01-13 | GSE216458 | GEO

Effects of bromodomain inhibitors on CD4 T+ cells under Th17-promoting conditions

Project description:The human dataset includes the gene expression profile of CD4+ T cells isolated from blood of healthy controls and plated on TCP in RPMI-1640 containing 10% FCS, Penicillin-Streptomycin (50,000 units-50 mg) and L-glutamine (2 mM). Cells were stimulated for 4 days with 20 ng/ml of IL-1beta, 100 IU/ml of IL-2, 20 ng/ml of IL-6, 20 ng/ml IL-23 plus anti-CD2/3/28 beads at a ratio of 1 bead per 10 cells. RNA samples were isolated using the RNeasy Mini Kit (Qiagen) with on-column DNA digestion. The transcriptional profile was evaluated in three different donors using the HT12v4.1 BeadChip arrays from Illumina.

2015-07-23 | GSE71231 | GEO

Gene array for identifying molecules involved in IL-10 regulation during Th17 polarization

Project description:IL-10 production by Th17 cells is critical for limiting autoimmunity and inflammatory responses. Gene array analysis on Stat6 and T-bet double deficient Th17 cells identified the Th2 transcription factor c-Maf to be synergistically up-regulated by IL-6 plus TGFbeta, and associated with Th17 IL-10 production. Both c-Maf and IL-10 induction during Th17 polarization depended on Stat3, but not Stat6 or Stat1, and mechanistically differed from IL-10 regulation by Th2 or IL-27 signals. TGFbeta was also synergistic with IL-27 to induce c-Maf, and induced Stat1 independent IL-10 expression in contrast to IL-27 alone. Retroviral transduction of c-Maf was able to induce IL-10 expression in Stat6 deficient CD4 and CD8 T cells, and c-Maf directly transactivated IL-10 gene expression through binding to a MARE motif in the IL-10 promoter. Together, these data reveal a novel role for c-Maf in regulating T effector development, and suggest that TGFbeta may antagonize Th17 immunity by IL-10 production through c-Maf induction. Our recent studies showed that IL-6 combined with TGFbeta differed from IL-6 combined with IL-23 for IL-10 production and pathogenic activities in CD4 T cells deficient in Stat6 and T-bet, despite similar IL-17 production. We performed gene array analysis on Stat6 and T-bet double deficient cells. We rationalized that by comparing gene expression in cells treated with IL-6 plus TGFbeta versus TGFbeta alone, we would be able to identify genes specific for standard Th17 polarization, and responsible for both IL-17 and IL-10 expression. By next comparing gene expression in cells treated with IL-6 plus TGFbeta versus IL-6 plus IL-23, we could eliminate molecules involved solely in IL-17 regulation, and obtain genes specifically responsible for IL-10 regulation.

2009-03-03 | E-GEOD-15029 | biostudies-arrayexpress

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