Abstract
Interleukin (IL)-4 and IL-13 share many biological activities. To some extent, this is because they both signal via a shared receptor, IL-4Rα. Ligation of IL-4Rα results in activation of Signal Transducer and Activator of Transcription factor 6 (STAT6) and Insulin Receptor Substrate (IRS) molecules. In T- and B-cells, IL- 4Rα signaling contributes to cell-mediated and humoral aspects of allergic inflammation. It has recently become clear that IL-4 and IL-13 produced in inflamed tissues activate signaling in normally resident cells of the airway. The purpose of this review is to critically evaluate the contributions of IL-4- and IL-13-induced tissue responses, especially those mediated by STAT6, to some of the pathologic features of asthma including eosinophilic inflammation, airway hyperresponsiveness, subepithelial fibrosis and excessive mucus production. We also review the functions of some recently identified IL-4- and/or IL-13-induced mediators that provide some detail on molecular mechanisms and suggest an important contribution to host defense.
Keywords: IL-4, IL-13, STAT6, allergy, asthma, inflammation, airway hyperresponsiveness, fibrosis, mucus
Current Molecular Medicine
Title: Interleukin-4, Interleukin-13, Signal Transducer and Activator of Transcription Factor 6, and Allergic Asthma
Volume: 8 Issue: 5
Author(s): Douglas A. Kuperman and Robert P. Schleimer
Affiliation:
Keywords: IL-4, IL-13, STAT6, allergy, asthma, inflammation, airway hyperresponsiveness, fibrosis, mucus
Abstract: Interleukin (IL)-4 and IL-13 share many biological activities. To some extent, this is because they both signal via a shared receptor, IL-4Rα. Ligation of IL-4Rα results in activation of Signal Transducer and Activator of Transcription factor 6 (STAT6) and Insulin Receptor Substrate (IRS) molecules. In T- and B-cells, IL- 4Rα signaling contributes to cell-mediated and humoral aspects of allergic inflammation. It has recently become clear that IL-4 and IL-13 produced in inflamed tissues activate signaling in normally resident cells of the airway. The purpose of this review is to critically evaluate the contributions of IL-4- and IL-13-induced tissue responses, especially those mediated by STAT6, to some of the pathologic features of asthma including eosinophilic inflammation, airway hyperresponsiveness, subepithelial fibrosis and excessive mucus production. We also review the functions of some recently identified IL-4- and/or IL-13-induced mediators that provide some detail on molecular mechanisms and suggest an important contribution to host defense.
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Cite this article as:
Kuperman A. Douglas and Schleimer P. Robert, Interleukin-4, Interleukin-13, Signal Transducer and Activator of Transcription Factor 6, and Allergic Asthma, Current Molecular Medicine 2008; 8 (5) . https://dx.doi.org/10.2174/156652408785161032
DOI https://dx.doi.org/10.2174/156652408785161032 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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