Control of RSV-induced lung injury by alternatively activated macrophages is IL-4R alpha-, TLR4-, and IFN-beta-dependent. - Wikidata - awgldk - TriplyDB

Control of RSV-induced lung injury by alternatively activated macrophages is IL-4R alpha-, TLR4-, and IFN-beta-dependent.

Control of RSV-induced lung injury by alternatively activated macrophages is IL-4R alpha-, TLR4-, and IFN-beta-dependent.

http://www.wikidata.org/entity/Q40734229

about

Lipoxins: nature's way to resolve inflammation The role of myeloid cell activation and arginine metabolism in the pathogenesis of virus-induced diseases The role of pro-resolution lipid mediators in infectious disease Macrophage proliferation, provenance, and plasticity in macroparasite infection Regulating the adaptive immune response to respiratory virus infection Critical role of TLR4 in human metapneumovirus mediated innate immune responses and disease pathogenesis Locally Produced IL-10 Limits Cutaneous Vaccinia Virus Spread Stimulation of immature lung macrophages with intranasal interferon gamma in a novel neonatal mouse model of respiratory syncytial virus infection Space and time: New considerations about the relationship between Toll-like receptors (TLRs) and type I interferons (IFNs)Specialized pro-resolving mediators: endogenous regulators of infection and inflammation Antiviral regulation in porcine monocytic cells at different activation states Macrophage plasticity and polarization: in vivo veritas Protective and pathogenic functions of macrophage subsets Macrophage activation and polarization: nomenclature and experimental guidelines A Role for Neutrophils in Viral Respiratory Disease.Viral infection of the lung: host response and sequelae Interaction between innate immunity and porcine reproductive and respiratory syndrome virus.Recent insights into pulmonary repair following virus-induced inflammation of the respiratory tract.Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.Macrophage polarization in inflammatory diseases.Macrophage activation state determines the response to rhinovirus infection in a mouse model of allergic asthma.Rapid host defense against Aspergillus fumigatus involves alveolar macrophages with a predominance of alternatively activated phenotype.The increased type-1 and type-2 chemokine levels in children with acute RSV infection alter the development of adaptive immune responses.New insights for development of a safe and protective RSV vaccine Agents that increase AAM differentiation blunt RSV-mediated lung pathology.Molecular mechanisms that influence the macrophage m1-m2 polarization balance.Macrophages as IL-25/IL-33-responsive cells play an important role in the induction of type 2 immunity.Nasally administered Lactobacillus rhamnosus strains differentially modulate respiratory antiviral immune responses and induce protection against respiratory syncytial virus infection Differential pathogenesis of respiratory syncytial virus clinical isolates in BALB/c mice.Genome-wide analysis of antiviral signature genes in porcine macrophages at different activation statuses.An essential role for TH2-type responses in limiting acute tissue damage during experimental helminth infection A genome-wide association study of asthma symptoms in Latin American children.Macrophage Polarization in Virus-Host Interactions Inflammatory responses to respiratory syncytial virus (RSV) infection and the development of immunomodulatory pharmacotherapeutics Regulation of inflammation by interleukin-4: a review of "alternatives"Genetic ablation of arginase 1 in macrophages and neutrophils enhances clearance of an arthritogenic alphavirus.Angiotensin-converting enzyme 2 inhibits lung injury induced by respiratory syncytial virus Interleukin-10 is a critical regulator of white matter lesion containment following viral induced demyelination An efferocytosis-induced, IL-4-dependent macrophage-iNKT cell circuit suppresses sterile inflammation and is defective in murine CGD Early infection with respiratory syncytial virus impairs regulatory T cell function and increases susceptibility to allergic asthma.

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P2860

Control of RSV-induced lung injury by alternatively activated macrophages is IL-4R alpha-, TLR4-, and IFN-beta-dependent.

http://www.wikidata.org/entity/Q40734229

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A C Puche

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A D Keegan

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G A Prince

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J C G Blanco

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K A Shirey

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L M Pletneva

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S N Vogel

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P2860

Respiratory syncytial virus infects and abortively replicates in the lungs in spite of preexisting immunity

Alternative activation of macrophages

Macrophage-specific PPARgamma controls alternative activation and improves insulin resistance

Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection.

Involvement of toll-like receptor 4 in innate immunity to respiratory syncytial virus.

Cox-2 inhibitors: today and tomorrow.

Toll-like receptor-induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens.

Review of epidemiology and clinical risk factors for severe respiratory syncytial virus (RSV) infection.

The pathogenesis of respiratory syncytial virus infection in cotton rats

Interleukin 4 potently enhances murine macrophage mannose receptor activity: a marker of alternative immunologic macrophage activation

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10.1038/MI.2010.6

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3

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3

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1052313139

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