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Expression data from MALP-2-stimulated macrophages from wild-type, IRAK-2-/- and IRAK-1-/IRAK-2-/- mice

ABSTRACT: IL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of IRAK-2 or IRAK-1/IRAK-2 deficiency in MALP-2-inducible gene expression. Keywords: Time course after MALP-2 stimulation

ORGANISM(S): Mus musculus

PROVIDER: GSE10765 | GEO | 2008/03/08

SECONDARY ACCESSION(S): PRJNA107553

REPOSITORIES: GEO

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Transcription profiling of mouse MALP-2-stimulated macrophages FROM wild-TYPE, IRAK-2-/- AND IRAK-1-/IRAK-2-/- animals

Project description:IL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of IRAK-2 or IRAK-1/IRAK-2 deficiency in MALP-2-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type, IRAK-2-/- and IRAK-1/IRAK-2 mice were stimulated with MALP-2 for 0, 2, 4, and 8 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2008-04-05 | E-GEOD-10765 | biostudies-arrayexpress

Transcription profiling of mouse embryonic fibroblasts from wild type and IRAK-4 kinase dead animals stimulated with IL-1b for different durations to identify IRAK-4 kinase-dependent IL-1b response genes.

Project description:IRAK-4 is an essential component of the signal transduction complex downstream of the IL-1- and Toll-like receptors. Though regarded as the first kinase in the signaling cascade, the role of IRAK-4 kinase activity versus its scaffold function is still controversial. In order to investigate the role of IRAK-4 kinase function in vivo, knock-in mice were generated by replacing the wild type IRAK-4 gene with a mutant gene encoding kinase deficient IRAK-4 protein (IRAK-4 KD). Analysis of embryonic fibroblasts and macrophages obtained from IRAK-4 KD mice with a number of experimental techniques demonstrated that they greatly lack responsiveness to stimulation with IL-1b or a Toll-like receptor 7 (TLR7) agonist. One of the techniques used, microarray analysis, identified IRAK-4 kinase-dependent IL-1b response genes in mouse embryonic fibroblasts and revealed that the induction of IL-1b-responsive mRNAs was largely ablated in IRAK-4 KD cells. In summary, our results suggest that IRAK-4 kinase activity plays a critical role in IL-1R/TLR7-mediated induction of inflammatory responses. Experiment Overall Design: The response of mouse embryonic fibroblasts from WT and IRAK4 kinase dead animals to stimulation with IL-1b at two time points was determined. There were 12 samples in total, 6 from WT and 6 from IRAK4 kinase dead cells; for each strain there were 3 conditions: growth for 4 hours without stimulation (the strain-specific control), growth for 1 hour with stimulation, and growth for 4 hours with stimulation; for each condition there were two biological replicates.

2007-11-15 | E-GEOD-6789 | biostudies-arrayexpress

Transcription profiling of responses to TNF-alpha, IL-1beta, peptidoglycan or lipopolysaccharide (TLR2/4 agonists) evaluated at 4 hrs in peripheral blood monocytes (PBM) from the patient bearing the IRAK4 Q293X mutation vs PBM from 5 healthy individuals

Project description:IL-1R associated kinase-4 (IRAK4) is a key enzyme required for activation of the common Toll-like Receptor (TLR) signaling cascade, which results in the transcription of inflammatory and immunity genes. IRAK-4 deficiency has recently been described as a rare form of innate immunodeficiency. Patients present with pyogenic bacterial infections and bacteraemia, particularly with Gram+ Streptococcus pneumoniae, and isolated PBMC from these patients fail to produce inflammatory cytokines in response to TLR agonists. We embarked on this study for several purposes: (1) to identify defective gene response resulting from IRAK4-deficiency that are responsible for the patients' susceptibility to infection by particular bacteria (2) to identify genetic responses that confer relatively normal immunity in these patients despite having a defect in such a critical component of the innate immune system (3) to gain understanding of the transcriptional regulation of inflammatory genes (4) to gain insight into TLR signal transduction pathways, in particular, the role of IRAK4 in the TLR2 and TLR4 pathways initiated by Gram+ and Gram- bacterial components respectively. Transcriptional responses to TNF-alpha, IL-1beta, peptidoglycan or lipopolysaccharide (TLR2/4 agonists) were evaluated at 4 hrs in peripheral blood monocytes (PBM) from the patient bearing the IRAK4 Q293X mutation compared to PBM from 5 healthy individuals.

2010-05-19 | E-FPMI-7 | biostudies-arrayexpress

IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans

2008-10-23 | GSE13300 | GEO

response to IL-1b of WT and IRAK4 kinase dead mouse embryonic fibroblasts

Project description:IRAK-4 is an essential component of the signal transduction complex downstream of the IL-1- and Toll-like receptors. Though regarded as the first kinase in the signaling cascade, the role of IRAK-4 kinase activity versus its scaffold function is still controversial. In order to investigate the role of IRAK-4 kinase function in vivo, ‘knock-in’ mice were generated by replacing the wild type IRAK-4 gene with a mutant gene encoding kinase deficient IRAK-4 protein (IRAK-4 KD). Analysis of embryonic fibroblasts and macrophages obtained from IRAK-4 KD mice with a number of experimental techniques demonstrated that they greatly lack responsiveness to stimulation with IL-1b or a Toll-like receptor 7 (TLR7) agonist. One of the techniques used, microarray analysis, identified IRAK-4 kinase-dependent IL-1b response genes in mouse embryonic fibroblasts and revealed that the induction of IL-1b-responsive mRNAs was largely ablated in IRAK-4 KD cells. In summary, our results suggest that IRAK-4 kinase activity plays a critical role in IL-1R/TLR7-mediated induction of inflammatory responses. Keywords: genetic modification, strain comparison, cell stimulation, time course, inflammatory response

2007-03-30 | GSE6789 | GEO

Transcription profiling of human single B cells isolated from patients deficient for IL-1R-associated kinase (IRAK)-4, myeloid differentiation factor 88 (MyD88) and UNC-93B

Project description:Most autoreactive B cells are normally counterselected during early B cell development. To determine whether Toll-like receptors (TLRs) regulate the removal of autoreactive B lymphocytes, we tested the reactivity of recombinant antibodies from single B cells isolated from patients deficient for IL-1R-associated kinase (IRAK)-4, myeloid differentiation factor 88 (MyD88) and UNC-93B. Indeed, all TLRs except TLR3 require IRAK-4 and MyD88 to signal and UNC-93B-deficient cells are unresponsive to TLR3, TLR7, TLR8 and TLR9. All patients suffered from defective central and peripheral B cell tolerance checkpoints resulting in the accumulation of large numbers of autoreactive mature naÃ¯ve B cells in their blood. Hence, TLR7, TLR8, and TLR9 may prevent the recruitment of developing autoreactive B cells in healthy donors. Paradoxically, IRAK-4-, MyD88- and UNC-93B-deficient patients did not display autoreactive antibodies in their serum nor developed autoimmune diseases, suggesting that IRAK-4, MyD88 and UNC-93B pathway blockade may thwart autoimmunity in humans. Experiment Overall Design: RNA was extracted from 105-3.105 batch sorted new emigrant and mature naÃ¯ve B cells isolated from donors using the Absolutely RNA microprep kit (Stratagene). 100-200 ng of RNA was obtained per sample, and the quality of the purified RNA was assessed by the Bioanalyzer from Agilent. Using the Ovation biotin system kit from Nugen, 30-50ng of RNA was amplified and labeled to produce cDNA. Labeled cDNA was hybridized on chips containing the whole human genome (Human Genome U133 2.0 from Affymetrix). Raw data from new emigrant (1 healthy donor) and mature naive (4 healthy donors) B cells were analyzed in order to determine the expression of some molecules involved in the TLR pathway in these B cell population in humans.

2008-11-13 | E-GEOD-13300 | biostudies-arrayexpress

Whole-Genome Gene Expression Bead Array analysis of Toll-like receptor 2/8 stimulated human monocytes

Project description:Monocytes and macrophages are essential cells in the early response in their capacity as ubiquitous phagocytic cells. They phagocytose microorganisms or damaged cells and sense pathogen/damage-associated molecular patterns (PAMPs/DAMPs) through innate receptors such as Toll-like receptors (TLRs). We investigated a phenomenon where co-signaling from TLR2 and TLR8 in human primary monocytes provides a distinct immune activation profile compared to signaling from either TLR alone. Comparison of gene signatures induced by either stimulus alone or together, show that co-signaling result in downstream differences in regulation of signaling and gene transcription. To investigate the interaction of TLR2 and TLR8 stimulation primary human monocytes isolated from buffy coat were stimulated with TLR2/6 ligand FSL-1 and/or TLR7/8 ligand CL075 and the gene expression monitored at 1,2 and 3h post stimulation.

2018-03-09 | E-MTAB-6222 | biostudies-arrayexpress

Expression data of LPS-stimulated macrophages from wild-type and Zc3h12a-/- mice.

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, induces the expression of various genes including proinflammatory cytokines, and the expression is modified by the presence of Zc3h12a. We used microarrays to examine influence of Zc3h12a deficiency in LPS-inducible gene expression. Keywords: Time course after LPS (100 ng/ml) stimulation

2009-02-19 | GSE14891 | GEO

Expression data of LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- mice.

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, activates intracellular signaling via adaptors, MyD88 and TRIF, leading to the expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of MyD88 or TRIF deficiency in LPS-inducible gene expression. Keywords: Time course after LPS (100 ng/ml) stimulation

2009-02-19 | GSE14890 | GEO

Inherited human IRAK-1 deficiency selectively abolishes TLR signaling in fibroblasts

Project description:We describe here a male infant with a 100 kb de novo Xq28 deletion encompassing parts of the TMEM187 and MECP2 protein-coding genes and the IRAK1 protein-coding gene, as well as the MIR3202-1, MIR3202-2, and MIR718 RNA-coding genes. We analyzed the impact of human IRAK-1 deficiency on a genome-wide gene expression in human fibroblasts in response to TLR2/6, TLR4 agonists as well as to IL-1β and TNF-α, using primary fibroblasts from healthy controls and IRAK-4-, MyD88- and MECP2-deficient patients for comparison.

2017-01-29 | GSE92466 | GEO

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