Persistence of asthma requires multiple feedback circuits involving type 2 innate lymphoid cells and IL-33. - Wikidata - wikimedia - TriplyDB

Persistence of asthma requires multiple feedback circuits involving type 2 innate lymphoid cells and IL-33.

Persistence of asthma requires multiple feedback circuits involving type 2 innate lymphoid cells and IL-33.

http://www.wikidata.org/entity/Q35828725

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Type 2 innate lymphoid cells: at the cross-roads in allergic asthma Insights into Group 2 Innate Lymphoid Cells in Human Airway Disease Management of the patient with eosinophilic asthma: a new era begins Group 2 innate lymphocytes (ILC2) are enriched in active eosinophilic esophagitis.Pulmonary receptor for advanced glycation end-products promotes asthma pathogenesis through IL-33 and accumulation of group 2 innate lymphoid cells Intrinsic functional defects of type 2 innate lymphoid cells impair innate allergic inflammation in promyelocytic leukemia zinc finger (PLZF)-deficient mice.Alternative splicing of interleukin-33 and type 2 inflammation in asthma.Emerging concepts and future challenges in innate lymphoid cell biology DUOX1 mediates persistent epithelial EGFR activation, mucous cell metaplasia, and airway remodeling during allergic asthma.IL-33 mediates reactive eosinophilopoiesis in response to airborne allergen exposure Accurately measuring and modeling Th2 and Th17 endotypes in severe asthma Serum IL-5 and IL-13 consistently serve as the best predictors for the blood eosinophilia phenotype in adult asthmatics.ILC2s and fungal allergy.Group 2 innate lymphoid cells in disease.Innate lymphoid cells: major players in inflammatory diseases.Leukotriene C4 Potentiates IL-33-Induced Group 2 Innate Lymphoid Cell Activation and Lung Inflammation.Oxidative Stress: Promoter of Allergic Sensitization to Protease Allergens?What rheumatologists need to know about innate lymphocytes.Airway epithelial dual oxidase 1 mediates allergen-induced IL-33 secretion and activation of type 2 immune responses.Regulation of IL-4 Expression in Immunity and Diseases.Revisiting Type 2-high and Type 2-low airway inflammation in asthma: current knowledge and therapeutic implications.Regulatory T cells and type 2 innate lymphoid cell-dependent asthma.PGI2 Controls Pulmonary NK Cells That Prevent Airway Sensitization to House Dust Mite Allergen.Allergic airway inflammation: key players beyond the Th2 cell pathway.Are ILC2s Jekyll and Hyde in airway inflammation?IL-33: biological properties, functions, and roles in airway disease.Innate lymphoid cells at the interface between obesity and asthma.Mucosal Type 2 Innate Lymphoid Cells Are a Key Component of the Allergic Response to Aeroallergens.Lung epithelium is the major source of IL-33 and is regulated by IL-33-dependent and IL-33-independent mechanisms in pulmonary cryptococcosis.Combinatorial targeting of TSLP, IL-25, and IL-33 in type 2 cytokine-driven inflammation and fibrosis.IL-27 suppresses type 2 immune responses in vivo via direct effects on group 2 innate lymphoid cells.HpARI Protein Secreted by a Helminth Parasite Suppresses Interleukin-33 β2 integrins rather than β1 integrins mediate Alternaria-induced group 2 innate lymphoid cell trafficking to the lung.MicroRNA regulation of type 2 innate lymphoid cell homeostasis and function in allergic inflammation.Strain Differences in a Murine Model of Air Pollutant-induced Nonatopic Asthma and Rhinitis.Group 2 Innate Lymphoid Cells Exhibit a Dynamic Phenotype in Allergic Airway Inflammation.Innate Lymphoid Cells (ILCs) as Mediators of Inflammation, Release of Cytokines and Lytic Molecules.Secreted PLA2 group X orchestrates innate and adaptive immune responses to inhaled allergen.IL-33 promotes the egress of group 2 innate lymphoid cells from the bone marrow.Role of group 2 innate lymphocytes in aspirin-exacerbated respiratory disease pathogenesis.

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Persistence of asthma requires multiple feedback circuits involving type 2 innate lymphoid cells and IL-33.

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J.JACI.2014.11.037

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The Journal of Allergy and Clinical Immunology

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Persistence of asthma requires ...... nate lymphoid cells and IL-33.

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Balachandra Gorentla

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Chaoyu Irvin

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Christina A Christianson

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Donald R Rollins

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HongWei Chu

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Iram Zafar

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James T Good

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Magdalena M Gorska

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Nicholas P Goplen

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Rafeul Alam

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P2860

Asthma: clinical expression and molecular mechanisms

Open cascades as simple solutions to providing ultrasensitivity and adaptation in cellular signaling

Transcription factor RORα is critical for nuocyte development

Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity

IL25 elicits a multipotent progenitor cell population that promotes T(H)2 cytokine responses

IL-33 is processed into mature bioactive forms by neutrophil elastase and cathepsin G

Signaling switches and bistability arising from multisite phosphorylation in protein kinase cascades

A positive-feedback-based bistable 'memory module' that governs a cell fate decision

IL-33 mediates inflammatory responses in human lung tissue cells

Innate production of T(H)2 cytokines by adipose tissue-associated c-Kit(+)Sca-1(+) lymphoid cells

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