Type II NKT cells stimulate diet-induced obesity by mediating adipose tissue inflammation, steatohepatitis and insulin resistance. - Wikidata - awgldk - TriplyDB

Type II NKT cells stimulate diet-induced obesity by mediating adipose tissue inflammation, steatohepatitis and insulin resistance.

Type II NKT cells stimulate diet-induced obesity by mediating adipose tissue inflammation, steatohepatitis and insulin resistance.

http://www.wikidata.org/entity/Q34181498

about

The Extended Family of CD1d-Restricted NKT Cells: Sifting through a Mixed Bag of TCRs, Antigens, and Functions I-L-C-2 it: type 2 immunity and group 2 innate lymphoid cells in homeostasis The immune system's involvement in obesity-driven type 2 diabetes The immune system as a sensor of the metabolic state Natural Killer T Cells Contribute to Neutrophil Recruitment and Ocular Tissue Damage in a Model of Intraocular Tumor Rejection Invariant natural killer T cells as sensors and managers of inflammation.Type II NKT-TFH cells against Gaucher lipids regulate B-cell immunity and inflammation The Response of CD1d-Restricted Invariant NKT Cells to Microbial Pathogens and Their Products Short term high fat diet challenge promotes alternative macrophage polarization in adipose tissue via natural killer T cells and interleukin-4.The inflammation highway: metabolism accelerates inflammatory traffic in obesity.Natural killer T cells in adipose tissue prevent insulin resistance Choline Deficiency Causes Colonic Type II Natural Killer T (NKT) Cell Loss and Alleviates Murine Colitis under Type I NKT Cell Deficiency.Natural killer T cells are required for lipopolysaccharide-mediated enhancement of atherosclerosis in apolipoprotein E-deficient mice.Natural killer and natural killer T cells in liver fibrosis A novel function of adipocytes in lipid antigen presentation to iNKT cells.Contribution of lipid-reactive natural killer T cells to obesity-associated inflammation and insulin resistance.Mechanisms of chronic state of inflammation as mediators that link obese adipose tissue and metabolic syndrome Adipose tissue invariant NKT cells protect against diet-induced obesity and metabolic disorder through regulatory cytokine production.Cutting edge: IL-25 elicits innate lymphoid type 2 and type II NKT cells that regulate obesity in mice.Mice lacking natural killer T cells are more susceptible to metabolic alterations following high fat diet feeding.Immunomodulatory type II natural killer T lymphocytes in health and disease.Immunological goings-on in visceral adipose tissue.Invariant natural killer T cells in adipose tissue: novel regulators of immune-mediated metabolic disease.Natural killer T cell based Immunotherapy.Immune cells and metabolic dysfunction.Morphological and inflammatory changes in visceral adipose tissue during obesity.Immunological mechanisms contributing to the double burden of diabetes and intracellular bacterial infections.From neutrophils to macrophages: differences in regional adipose tissue depots.Natural killer T cells in atherosclerosis.Unusual Suspects in the Development of Obesity-Induced Inflammation and Insulin Resistance: NK cells, iNKT cells, and ILCs.CD301b(+) Mononuclear Phagocytes Maintain Positive Energy Balance through Secretion of Resistin-like Molecule Alpha.Communication between natural killer T cells and adipocytes in obesity.Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice.Endogenous lipid antigens for invariant Natural Killer T cells hold the reins in adipose tissue homeostasis.A Novel Mouse Model of iNKT Cell-deficiency Generated by CRISPR/Cas9 Reveals a Pathogenic Role of iNKT Cells in Metabolic Disease.From lung to liver: how does airborne particulate matter trigger NASH and systemic insulin resistance?Deficiency of Invariant Natural Killer T Cells Does Not Protect Against Obesity but Exacerbates Atherosclerosis in Ldlr-/- Mice.Maternal obesity associated with increase in natural killer T cells and CD8+ regulatory T cells in cord blood units.Adipocyte CD1d determines adipose inflammation and insulin resistance in obesity.M2-specific reduction of CD1d switches NKT cell-mediated immune responses and triggers metaflammation in adipose tissue.

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Type II NKT cells stimulate diet-induced obesity by mediating adipose tissue inflammation, steatohepatitis and insulin resistance.

http://www.wikidata.org/entity/Q34181498

description

2012 nî lūn-bûn

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2012 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2012年の論文

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Type II NKT cells stimulate di ...... atitis and insulin resistance.

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Type II NKT cells stimulate di ...... atitis and insulin resistance.

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Type II NKT cells stimulate di ...... atitis and insulin resistance.

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Christopher Stuart Clingan

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Hiroyuki Tsutsui

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Hisako Ogura

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Kazunori Onoé

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Kazuya Iwabuchi

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Koji Eshima

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Masaru Taniguchi

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Masashi Satoh

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Naoki Ishimori

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Noriyuki Hirata

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P2860

Monitoring bacterial community of human gut microbiota reveals an increase in Lactobacillus in obese patients and Methanogens in anorexic patients

B cells promote insulin resistance through modulation of T cells and production of pathogenic IgG antibodies

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance

Eosinophils sustain adipose alternatively activated macrophages associated with glucose homeostasis

Inflammation and metabolic disorders

Obesity is associated with macrophage accumulation in adipose tissue

The gut microbiota as an environmental factor that regulates fat storage

CD1d-restricted and TCR-mediated activation of valpha14 NKT cells by glycosylceramides

CD1d1 mutant mice are deficient in natural T cells that promptly produce IL-4

Obesity induces a phenotypic switch in adipose tissue macrophage polarization

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2

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Toshinori Nakayama

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221882567

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Steatohepatitis

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3284453

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