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| http://dx.doi.org/10.1016/j.jaci.2016.12.954 | DOI Listing |
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Allergen-dependent oxidant formation requires purinoceptor activation of ADAM 10 and prothrombin.
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Institute for Infection and Immunity, St George's, University of London, London, United Kingdom. Electronic address:
Defining the molecular role of gp91phox in the immune manifestation of acute allergic asthma using a preclinical murine model.
Clin Mol Allergy
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Department of Medicine, Division of Allergy and Infectious Diseases, Center for Allergy and Inflammation, University of Washington, Room 254, 815 Mercer Street, Seattle, WA 98195, USA.
Objective: The phenomena manifested during inflammation require interplay between circulating effector cells, local resident cells, soluble mediators and genetic host factors to establish, develop and maintain itself. Of the molecues involed in the initiation and perpetuation of acute allergic inflammation in asthma, the involvement of effector cells in redox reactions for producing O2- (superoxide anion) through the mediation of NADPH oxidase is a critical step. Prior data suggest that reactive oxygen species (ROS) produced by NADPH oxidase homologues in non-phagocytic cells play an important role in the regulation of signal transduction, while macrophages use a membrane-associated NADPH oxidase to generate an array of oxidizing intermediates which inactivate MMPs on or near them.
View Article and Find Full Text PDFInducible nitric oxide synthase and proinflammatory cytokine expression by human keratinocytes during acute urticaria.
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Department of Immunology (Molecular Immuno-Hematology Group), University of Paris VI, College of Medicine, France.
Background: IgE/allergen-dependent activation of skin mast cells is involved in acute urticaria and leads to their IL-4 release. Previously we have demonstrated in vitro the induction of the low-affinity receptor for IgE (CD23/Fc epsilon RII) in human keratinocytes (HK) upon stimulation with IL-4. In addition, we have observed that ligation of CD23 on keratinocytes induced type II nitric oxide synthase (iNOS), leading to the release of nitric oxide (NO) and proinflammatory cytokines (TNF-alpha, IL-6).
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