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Th2 cells and cytokine networks in allergic inflammation of the lung

The cytokines released from Th2 and Th2-like cells are likely to be central to the pathophysiolgy of asthma and allergy, contributing to aberrant IgE production, eosinophilia and, perhaps, mucosal susceptibility to viral infection. IL-4 has emerged as a central target, not only for B cell IgE produc...

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Detalles Bibliográficos
Autores principales: Coyle, Anthony J., Tsuyuki, Shogo
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 1995
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365650/
https://www.ncbi.nlm.nih.gov/pubmed/18475645
http://dx.doi.org/10.1155/S096293519500038X
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author Coyle, Anthony J.
Tsuyuki, Shogo
author_facet Coyle, Anthony J.
Tsuyuki, Shogo
author_sort Coyle, Anthony J.
collection PubMed
description The cytokines released from Th2 and Th2-like cells are likely to be central to the pathophysiolgy of asthma and allergy, contributing to aberrant IgE production, eosinophilia and, perhaps, mucosal susceptibility to viral infection. IL-4 has emerged as a central target, not only for B cell IgE production, but also in the commitment of both CD4+ and CD8+ T cells to cells with Th2 effector function capable of secreting IL-5 resultlng in eosinophilic inflammation. In view of the central role of this cytokine and the evidence that glucocorticoids are unable to modify many IL-4 dependent effects, Th2 inhibitors may prove to be novel therapies for the treatment of bronchial asthma.
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spelling pubmed-23656502008-05-12 Th2 cells and cytokine networks in allergic inflammation of the lung Coyle, Anthony J. Tsuyuki, Shogo Mediators Inflamm Research Article The cytokines released from Th2 and Th2-like cells are likely to be central to the pathophysiolgy of asthma and allergy, contributing to aberrant IgE production, eosinophilia and, perhaps, mucosal susceptibility to viral infection. IL-4 has emerged as a central target, not only for B cell IgE production, but also in the commitment of both CD4+ and CD8+ T cells to cells with Th2 effector function capable of secreting IL-5 resultlng in eosinophilic inflammation. In view of the central role of this cytokine and the evidence that glucocorticoids are unable to modify many IL-4 dependent effects, Th2 inhibitors may prove to be novel therapies for the treatment of bronchial asthma. Hindawi Publishing Corporation 1995-07 /pmc/articles/PMC2365650/ /pubmed/18475645 http://dx.doi.org/10.1155/S096293519500038X Text en Copyright © 1995 Hindawi Publishing Corporation. http://creativecommons.org/licenses/by/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Coyle, Anthony J.
Tsuyuki, Shogo
Th2 cells and cytokine networks in allergic inflammation of the lung
title Th2 cells and cytokine networks in allergic inflammation of the lung
title_full Th2 cells and cytokine networks in allergic inflammation of the lung
title_fullStr Th2 cells and cytokine networks in allergic inflammation of the lung
title_full_unstemmed Th2 cells and cytokine networks in allergic inflammation of the lung
title_short Th2 cells and cytokine networks in allergic inflammation of the lung
title_sort th2 cells and cytokine networks in allergic inflammation of the lung
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365650/
https://www.ncbi.nlm.nih.gov/pubmed/18475645
http://dx.doi.org/10.1155/S096293519500038X
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