Extracellular high-mobility group box 1 acts as an innate immune mediator to enhance autoimmune progression and diabetes onset in NOD mice - Wikidata - wikimedia - TriplyDB

Extracellular high-mobility group box 1 acts as an innate immune mediator to enhance autoimmune progression and diabetes onset in NOD mice

Extracellular high-mobility group box 1 acts as an innate immune mediator to enhance autoimmune progression and diabetes onset in NOD mice

http://www.wikidata.org/entity/Q36807621

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Disruption of a Regulatory Network Consisting of Neutrophils and Platelets Fosters Persisting Inflammation in Rheumatic Diseases Trauma equals danger--damage control by the immune system HMGB1 conveys immunosuppressive characteristics on regulatory and conventional T cells The dendritic cell response to classic, emerging, and homeostatic danger signals. Implications for autoimmunity The role of dendritic cells in autoimmunity Loss of Jak2 selectively suppresses DC-mediated innate immune response and protects mice from lethal dose of LPS-induced septic shock.HMGB1 in health and disease.Comparative analysis of the alveolar macrophage proteome in ALI/ARDS patients between the exudative phase and recovery phase.Low shear stress induced HMGB1 translocation and release via PECAM-1/PARP-1 pathway to induce inflammation response T cell-driven initiation and propagation of autoimmune diabetes The Free Radical Scavenger NecroX-7 Attenuates Acute Graft-versus-Host Disease via Reciprocal Regulation of Th1/Regulatory T Cells and Inhibition of HMGB1 Release.Relationship of Soluble RAGE with Insulin Resistance and Beta Cell Function during Development of Type 2 Diabetes Mellitus.The role of endoplasmic reticulum stress in autoimmune-mediated beta-cell destruction in type 1 diabetes.Cx3cr1 deficiency in mice attenuates hepatic granuloma formation during acute schistosomiasis by enhancing the M2-type polarization of macrophages NO donor induces Nec-1-inhibitable, but RIP1-independent, necrotic cell death in pancreatic β-cells.Toll-like receptor 4 on islet β cells senses expression changes in high-mobility group box 1 and contributes to the initiation of type 1 diabetes Chop deficiency prevents UUO-induced renal fibrosis by attenuating fibrotic signals originated from Hmgb1/TLR4/NFκB/IL-1β signaling.AAL exacerbates pro-inflammatory response in macrophages by regulating Mincle/Syk/Card9 signaling along with the Nlrp3 inflammasome assembly.Transcriptomic analysis of the effects of Toll-like receptor 4 and its ligands on the gene expression network of hepatic stellate cells Protective Effect of an Antibody against Specific Extracellular Domain of TLR2 on Agonists-Driven Inflammatory and Allergic Response SUMO1 regulates endothelial function by modulating the overall signals in favor of angiogenesis and homeostatic responses HMGB1 exacerbates bronchiolitis obliterans syndrome via RAGE/NF-κB/HPSE signaling to enhance latent TGF-β release from ECM.HMGB1, an innate alarmin, in the pathogenesis of type 1 diabetes.The Role of HMGB1 in the Pathogenesis of Type 2 Diabetes.Tim-1-Fc suppresses chronic cardiac allograft rejection and vasculopathy by reducing IL-17 production Pdx1 and other factors that regulate pancreatic beta-cell survival.HMGB1 is an early and critical mediator in an animal model of uveitis induced by IRBP-specific T cells.HMGB1, TLR and RAGE: a functional tripod that leads to diabetic inflammation.High-mobility group box-1 in sterile inflammation.How apoptotic β-cells direct immune response to tolerance or to autoimmune diabetes: a review.The influence of the telomere-telomerase system on diabetes mellitus and its vascular complications.Inhibition of high-mobility group box 1 expression by siRNA in rat hepatic stellate cells Receptor for Advanced Glycation End Products (RAGE) in Type 1 Diabetes Pathogenesis.The role of Toll-like receptor proteins (TLR) 2 and 4 in mediating inflammation in proximal tubules.Niaspan reduces high-mobility group box 1/receptor for advanced glycation endproducts after stroke in type-1 diabetic rats High-mobility group box 1 protein (HMGB1) neutralization ameliorates experimental autoimmune encephalomyelitis.Neutralization of the extracellular HMGB1 released by ischaemic damaged renal cells protects against renal ischaemia-reperfusion injury.High-mobility group box 1 promotes early acute allograft rejection by enhancing IL-6-dependent Th17 alloreactive response.Both conditional ablation and overexpression of E2 SUMO-conjugating enzyme (UBC9) in mouse pancreatic beta cells result in impaired beta cell function.Cellular death, reactive oxygen species (ROS) and diabetic complications.

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Extracellular high-mobility group box 1 acts as an innate immune mediator to enhance autoimmune progression and diabetes onset in NOD mice

http://www.wikidata.org/entity/Q36807621

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2008年论文

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Extracellular high-mobility gr ...... and diabetes onset in NOD mice

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Extracellular high-mobility gr ...... and diabetes onset in NOD mice

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Extracellular high-mobility gr ...... and diabetes onset in NOD mice

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Cong-Yi Wang

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David M Stern

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Feili Gong

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Jin-Xiong She

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Junyan Han

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Mong-Heng Wang

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Ping Yang

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Sharad Purohit

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Wenzhong Wei

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Yafei Huang

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P2860

Release of high mobility group box 1 by dendritic cells controls T cell activation via the receptor for advanced glycation end products

Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

HMG-1 as a late mediator of endotoxin lethality in mice

SUMO wrestling with type 1 diabetes

The secretion of HMGB1 is required for the migration of maturing dendritic cells

Genetic and functional evidence supporting SUMO4 as a type 1 diabetes susceptibility gene

Toll-like receptors and other links between innate and acquired alloimmunity.

Role of Toll-like receptor-driven innate immunity in thoracic organ transplantation.

SUMO4 and its role in type 1 diabetes pathogenesis.

Unusual resistance of ALR/Lt mouse beta cells to autoimmune destruction: role for beta cell-expressed resistance determinants

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10.2337/DB07-1499

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18477810

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2494682

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