Loss of NADPH oxidase-derived superoxide skews macrophage phenotypes to delay type 1 diabetes - Wikidata - awgldk - TriplyDB

Loss of NADPH oxidase-derived superoxide skews macrophage phenotypes to delay type 1 diabetes

Loss of NADPH oxidase-derived superoxide skews macrophage phenotypes to delay type 1 diabetes

http://www.wikidata.org/entity/Q35114505

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The Reactive Oxygen Species in Macrophage Polarization: Reflecting Its Dual Role in Progression and Treatment of Human Diseases The role of oxidative stress in skeletal muscle injury and regeneration: focus on antioxidant enzymes Islet encapsulation with polyphenol coatings decreases pro-inflammatory chemokine synthesis and T cell trafficking Inhibition of NADPH oxidase activation reduces EAE-induced white matter damage in mice.Macrophage Differentiation from Monocytes Is Influenced by the Lipid Oxidation Degree of Low Density Lipoprotein.Loss of NOX-Derived Superoxide Exacerbates Diabetogenic CD4 T-Cell Effector Responses in Type 1 Diabetes The Metabolic Prospective and Redox Regulation of Macrophage Polarization.Berberine Inhibits Intestinal Polyps Growth in Apc (min/+) Mice via Regulation of Macrophage Polarization.Downregulation of vimentin in macrophages infected with live Mycobacterium tuberculosis is mediated by Reactive Oxygen Species.Are reactive oxygen species still the basis for diabetic complications?Microglia antioxidant systems and redox signalling.The IRAK-ERK-p67phox-Nox-2 axis mediates TLR4, 2-induced ROS production for IL-1β transcription and processing in monocytes Reactive oxygen homeostasis - the balance for preventing autoimmunity.Ethyl Acetate Extract of Origanum vulgare L. ssp. hirtum Prevents Streptozotocin-Induced Diabetes in C57BL/6 Mice.NADPH Oxidase-Derived Superoxide Provides a Third Signal for CD4 T Cell Effector Responses.Deficiency in the voltage-gated proton channel Hv1 increases M2 polarization of microglia and attenuates brain damage from photothrombotic ischemic stroke.Age increases reactive oxygen species production in macrophages and potentiates oxidative damage after spinal cord injury.Polarization of Macrophages toward M2 Phenotype Is Favored by Reduction in iPLA2β (Group VIA Phospholipase A2)Redox-Sensitive Innate Immune Pathways During Macrophage Activation in Type 1 Diabetes.T Cell-Mediated Beta Cell Destruction: Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes.Superoxide Production by NADPH Oxidase Intensifies Macrophage Antiviral Responses during Diabetogenic Coxsackievirus Infection.Mitochondrial Reactive Oxygen Species and Type 1 Diabetes.

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P2860

Loss of NADPH oxidase-derived superoxide skews macrophage phenotypes to delay type 1 diabetes

http://www.wikidata.org/entity/Q35114505

description

2014 nî lūn-bûn

@nan

2014 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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Loss of NADPH oxidase-derived ...... types to delay type 1 diabetes

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Ashley R Burg

http://www.w3.org/2001/XMLSchema#string

Hubert M Tse

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Lindsey E Padgett

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Weiqi Lei

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P2860

IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses

Macrophage plasticity and polarization: in vivo veritas

The chemokine system in diverse forms of macrophage activation and polarization

Alternative activation of macrophages: an immunologic functional perspective

IFN-gamma-dependent regulatory circuits in immune inflammation highlighted in diabetes.

Mononuclear cell infiltration and its relation to the expression of major histocompatibility complex antigens and adhesion molecules in pancreas biopsy specimens from newly diagnosed insulin-dependent diabetes mellitus patients.

Biological defense mechanisms. The production by leukocytes of superoxide, a potential bactericidal agent.

Superoxide production by macrophages and T cells is critical for the induction of autoreactivity and type 1 diabetes

NADPH oxidase deficiency regulates Th lineage commitment and modulates autoimmunity.

In CD4+ T-cell-induced diabetes, macrophages are the final effector cells that mediate islet beta-cell killing: studies from an acute model.

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937-946

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10.2337/DB14-0929

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type-1 diabetes

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