Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA200304 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome wide expression study of the effect of single stranded RNA (ssRNA) in A/JOlaHsd (WT), A/J and A/J-MyD88 deficient mice. The hypothesis for this study was that endogenous TLR ligands released from the leaking dysferlin-deficient muscle fibers engage TLRs on muscle and immune cells and contribute to disease progression.These data point to a clear role for the TLR pathway in the pathogenesis of dysferlin deficiency.
2013-04-27 | GSE46420 | GEO
Project description:Genome wide expression study of the effect of single stranded RNA (ssRNA) in A/JOlaHsd (WT), A/J and A/J-MyD88 deficient mice. The hypothesis for this study was that endogenous TLR ligands released from the leaking dysferlin-deficient muscle fibers engage TLRs on muscle and immune cells and contribute to disease progression.These data point to a clear role for the TLR pathway in the pathogenesis of dysferlin deficiency. Total RNA obtained from isolated tibalis anterior muscles (TA) of A/JOlaHsd (WT), A/J and A/J-MyD88 deficient mice that were subjected to 3 intramuscular injections of ssRNA over the period of 10 days compared to their contraleteral legs that were injected with saline (control).
2013-04-27 | E-GEOD-46420 | biostudies-arrayexpress
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. Experiment Overall Design: Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.
2009-03-01 | E-GEOD-14890 | biostudies-arrayexpress
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
Project description:Human intestinal macrophages contribute to tissue homeostasis in noninflamed mucosa through profound down-regulation of pro-inflammatory cytokine release. Here, we show that this down-regulation extends to Toll-like receptor (TLR)-induced cytokine release, as intestinal macrophages expressed TLR3-TLR9 but did not release cytokines in response to TLR-specific ligands. Likely contributing to this unique functional profile, intestinal macrophages expressed markedly down-regulated adapter proteins MyD88 and Toll interleukin receptor 1 domain-containing adapter-inducing interferon beta, which together mediate all TLR MyD88-dependent and -independent NF-kappaB signaling, did not phosphorylate NF-kappaB p65 or Smad-induced IkappaBalpha, and did not translocate NF-kappaB into the nucleus. Importantly, transforming growth factor-beta released from intestinal extracellular matrix (stroma) induced identical down-regulation in the NF-kappaB signaling and function of blood monocytes, the exclusive source of intestinal macrophages. Our findings implicate stromal transforming growth factor-beta-induced dysregulation of NF-kappaB proteins and Smad signaling in the differentiation of pro-inflammatory blood monocytes into noninflammatory intestinal macrophages. Comparison of unstimulated monocytes and macrophages, and flagellin stimulated monocytes and macrophages.
2010-07-07 | E-GEOD-22373 | biostudies-arrayexpress
Project description:Transcriptome analysis of submandibular glands in female MyD88+/+ and MyD88−/− NOD mice. Sjögren's syndrome (SS) is an autoimmune disease characterized by dysfunction of salivary glands (SGs) and lacrimal glands, which is caused by chronic inflammation associated with autoantibody and autoreactive lymphocyte infiltration. The pathogenic mechanism of SS has not been fully elucidated. Infiltrated lymphocytes form regularized structures similar to lymphoid follicles of secondary lymphoid organs, such as T/B cell compartments, high endothelial venules (HEVs), lymphatic vessels, and germinal centers, therefore being believed as an ectopic lymphoid tissue called tertiary lymphoid organs (TLO). We previously found that deletion of the Toll-like receptor/IL-1 receptor (TLR/IL-1R) adaptor molecule gene Myd88 in SS model mice NOD reduced the frequency of lymphocyte infiltration and HEV formation in SGs. In this study, we analyzed the effect of MyD88 deficiency on lymphoid follicle formation in SGs of NOD mice. Microarray analysis showed decreased expression of genes related to TLO, such as Cxcl13 and Cxcr5, in Myd88-deficient SGs. These results indicate that deficiency of TLR/IL-1R signaling decrease gene expression ot chemokines in SGs, suggesting MyD88-dependent signaling is directly involved in formation of lymphoid follicles in SS.
2021-09-01 | GSE157669 | GEO
Project description:Toll-like Receptors (TLRs) are key mediators of immune responses to infection. Upon microbial detection, these receptors activate inflammatory signal transduction pathways that involve IκB kinases, mitogen activated protein kinases, ubiquitin ligases and other adaptor proteins. Current models suggest these signaling proteins operate within functionally distinct multiprotein complexes, which are all activated by a receptor-proximal complex known as the myddosome. The mechanisms that connect the effector protein complexes in the TLR pathways are undefined. To define TLR pathway activities, we engineered macrophages to enable proteomic analysis of the endogenous myddosome constituent MyD88 and its interacting proteins. Proteomics demonstrated that myddosomes contain proteins that act at all stages and regulate all effector responses of the TLR signaling pathways.
2024-07-04 | PXD047416 | Pride
Project description:Human intestinal macrophages contribute to tissue homeostasis in noninflamed mucosa through profound down-regulation of pro-inflammatory cytokine release. Here, we show that this down-regulation extends to Toll-like receptor (TLR)-induced cytokine release, as intestinal macrophages expressed TLR3-TLR9 but did not release cytokines in response to TLR-specific ligands. Likely contributing to this unique functional profile, intestinal macrophages expressed markedly down-regulated adapter proteins MyD88 and Toll interleukin receptor 1 domain-containing adapter-inducing interferon beta, which together mediate all TLR MyD88-dependent and -independent NF-kappaB signaling, did not phosphorylate NF-kappaB p65 or Smad-induced IkappaBalpha, and did not translocate NF-kappaB into the nucleus. Importantly, transforming growth factor-beta released from intestinal extracellular matrix (stroma) induced identical down-regulation in the NF-kappaB signaling and function of blood monocytes, the exclusive source of intestinal macrophages. Our findings implicate stromal transforming growth factor-beta-induced dysregulation of NF-kappaB proteins and Smad signaling in the differentiation of pro-inflammatory blood monocytes into noninflammatory intestinal macrophages.
2010-06-22 | GSE22373 | GEO
Project description:The objective of this study is to: 1) Characterize the innate immune responsiveness of patients with inborn errors in Toll-IL1 receptor signaling pathway (IRAK4, MyD88 deficiencies) compared to healthy subjects, through the analysis of blood leukocytes' transcriptional profiles after stimulation with ligands for the whole set of Toll-like receptors and IL-1Rs plus whole bacteria. 2) Understand the redundancies in TLR pathway in humans. 3) Explore the use of blood profiling approaches to assess the immune status of an individual by using Primary Immune Deficiencies as a proof of principle.
2014-10-26 | GSE25742 | GEO
Project description:To investigate the similarity of toll-like receptor tolerance in macrophages stimulated with different toll-like receptor ligands we stimulated naïve or tolerant macrophages with ligands for TLR4, TLR2, TLR3 and TLR9. The data identifies a core set of genes that are tolerised by all ligands and genes that show TLR specific patterns.
2018-05-30 | GSE81291 | GEO