Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA293673 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:PPAR/ ligand response in monocyte derived macrophages
2025-01-23 | E-MTAB-3398 | ExpressionAtlas
Project description:In this study we used bioluminescent reporter mice to discover that transplantable tumors cause nuclear factor-kappa B activation in host macrophages. This effect is mostly aggravated in mouse models of malignant pleural effusion, is dependent on KRAS mutation status of tumor cells, and is delivered via secretory versican, a toll-like receptor 2 ligand. Versican, in turn activates nuclear factor-kappa B in host macrophages via the canonical inhibitor of nuclear factor-kappa B kinase beta (IKKbeta), resulting in release of myeloid-secreted interleukin-1beta in the tumor microenvironment. Silencing of versican in cancer cells or conditional deletion of IKKbeta in macrophages abrogates myeloid nuclear factor-kappa B activation as well as tumor progression.
2025-05-02 | GSE130716 | GEO
Project description:Bone marrow derived cells stimulated with RANKL (receptor activator of nuclear factor kappa B ligand, also known as Tumor necrosis factor ligand superfamily member 11) to generate osteoclasts.
2007-06-06 | E-TABM-212 | biostudies-arrayexpress
Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is on the rise, and with limited pharmacological therapy available, identification of new metabolic targets is urgently needed. Oxalate is a terminal metabolite produced from glyoxylate by lactate dehydrogenase (LDHA). The liver-specific alanine-glyoxylate aminotransferase (AGXT) detoxifies glyoxylate, preventing oxalate accumulation. We report that AGXT is suppressed and LDHA is activated in livers from patients and mice with MASH, leading to oxalate overproduction. In turn, oxalate promotes steatosis in hepatocytes by inhibiting peroxisome proliferator activated receptor-alpha (PPARa) transcription and fatty acid b-oxidation (FAO), and induces monocyte chemotaxis via C-C motif chemokine ligand 2. In male mice with diet-induced MASH, blocking oxalate overproduction through hepatocyte-specific AGXT overexpression or pharmacological inhibition of LDHA potently lower steatosis, inflammation, and fibrosis by inducing PPARa-driven FAO, and suppressing monocyte chemotaxis, nuclear factor-kappa B and transforming growth factor-beta targets. These findings highlight hepatic oxalate overproduction as a new target for the treatment of MASH.
2024-04-21 | MSV000094587 | MassIVE
Project description:Increased antigen cross-presentation but impaired cross-priming after activation of PPARγ is mediated by up-regulation of B7H1 Dendritic cells (DCs) are able to take up exogenous antigens and present antigen-derived peptides on MHC class I molecules, a process termed cross-presentation. The mannose receptor (MR), an endocytic receptor expressed on a variety of antigen-presenting cells (APCs), has been demonstrated to target soluble antigens exclusively towards cross-presentation. In this study, we investigated the role of the murine nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ), a ligand-activated transcription factor with immunomodulatory properties, in MR-mediated endocytosis and cross-presentation of the model antigen ovalbumin (OVA). We could demonstrate both in vitro and in vivo that activation of PPARγ resulted in increased MR expression, which in consequence led to enhanced MR-mediated endocytosis and elevated cross-presentation of soluble OVA. Concomitantly, activation of PPARγ in DCs induced up-regulation of the co-inhibitory molecule B7H1, which, despite enhanced cross-presentation, caused an impaired activation of naive OVA-specific CD8+ T cells and the induction of T cell tolerance. These data provide a mechanistic basis for the immunomodulatory action of PPARγ which might open new possibilities in development of therapeutical approaches aimed at the control of excessive immune responses, e.g. in T cell-mediated autoimmunity. Comparison of murine mannose receptor negative versus mannose receptor positive bone marrow-derived DCs
2010-05-08 | E-GEOD-15616 | biostudies-arrayexpress
Project description:Emerging studies revealed an immunomodulatory role of the Aryl hydrocarbon receptor (AhR), a receptor sensing environmental contaminants, and involved in their detoxification. Besides its function as a transcription factor, AhR can participate in non-genomic signaling through ubiquitination and phosphorylation-dependent processes. In this study, a multi-PTM-omics approach, including proteome, ubiquitome, and phosphoproteome, was utilized to examine mechanisms of non-genomic AhR-signaling in endotoxin-activated monocyte-derived macrophages. This dataset entails proteome and phosphoproteome data.
2021-03-30 | PXD020770 | Pride
Project description:Increased antigen cross-presentation but impaired cross-priming after activation of PPARγ is mediated by up-regulation of B7H1 Dendritic cells (DCs) are able to take up exogenous antigens and present antigen-derived peptides on MHC class I molecules, a process termed cross-presentation. The mannose receptor (MR), an endocytic receptor expressed on a variety of antigen-presenting cells (APCs), has been demonstrated to target soluble antigens exclusively towards cross-presentation. In this study, we investigated the role of the murine nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ), a ligand-activated transcription factor with immunomodulatory properties, in MR-mediated endocytosis and cross-presentation of the model antigen ovalbumin (OVA). We could demonstrate both in vitro and in vivo that activation of PPARγ resulted in increased MR expression, which in consequence led to enhanced MR-mediated endocytosis and elevated cross-presentation of soluble OVA. Concomitantly, activation of PPARγ in DCs induced up-regulation of the co-inhibitory molecule B7H1, which, despite enhanced cross-presentation, caused an impaired activation of naive OVA-specific CD8+ T cells and the induction of T cell tolerance. These data provide a mechanistic basis for the immunomodulatory action of PPARγ which might open new possibilities in development of therapeutical approaches aimed at the control of excessive immune responses, e.g. in T cell-mediated autoimmunity.
2009-06-19 | GSE15616 | GEO
Project description:Overall goal was to look for the differentially expressed genes between receptor activator of nuclear factor kappa-B ligand (RANKL)-stimulated wild type (WT) bone marrow macrophages (BMMs) and the BMMs in which the expression or the enzyme activity of cyclooxygenase-2 (Cox2), the major enzyme for prostaglandin E2 (PGE2) synthesis, is absent. For this purpose, two separate microarrays (experiment 1 and 2) were done. In both the experiments, Serum Amyloid A3 (Saa3) was one of the most highly differentially expressed gene.
2016-01-07 | GSE72047 | GEO
Project description:Transcription profiling of peripheral blood monocyte derived macrophages treated or not with synthetic REVERB ligand GSK-4112.
2025-01-23 | E-MTAB-6478 | ExpressionAtlas
Project description:Toll-like receptor (TLR) signalling activation by pathogens is critical to the induction of immune responses, and demands tight regulation. Chemokine ligand 2 (CCL2) secretion triggered by TLR4 or TLR8 engagement is strongly inhibited upon simultaneous activation of both TLRs in human monocyte-derived dendritic cells (MD-DC). Impaired CCL2 secretion occurs concomitantly to IL-12 up-regulation, being part of a complex regulatory circuit ensuring optimal Th type 1 polarization. Interestingly, triggering selected TLRs or their combinations differently affects nuclear factor-kB p65 activation and microRNA expression. To investigate in details such different modulation we performed a microarray profiling of MD-DCs stimulated by different TLRs agonist or their combination in three different donors. We found that CCL2 supplies an important immunomodulatory role to DCs, and may contribute to dictate the cytokine profile in Th type 1 responses induced by DCs.
2009-05-22 | E-MEXP-2183 | biostudies-arrayexpress