IgE alone promotes human lung mast cell survival through the autocrine production of IL-6

<p>Abstract</p> <p>Background</p> <p>Mast cells play a key role in asthma and recent evidence indicates that their ongoing activation in this disease is mediated, in part, <it>via </it>IgE in the absence of antigen. In this study we have examined whether IgE...

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Main Authors: Cockerill Sarah, Cruse Glenn, Bradding Peter
Format: Article
Language:English
Published: BMC 2008-01-01
Series:BMC Immunology
Online Access:http://www.biomedcentral.com/1471-2172/9/2
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spelling doaj-8a2e99e954d4470383b2bd6f9bdc2aaf2020-11-25T01:38:55ZengBMCBMC Immunology1471-21722008-01-0191210.1186/1471-2172-9-2IgE alone promotes human lung mast cell survival through the autocrine production of IL-6Cockerill SarahCruse GlennBradding Peter<p>Abstract</p> <p>Background</p> <p>Mast cells play a key role in asthma and recent evidence indicates that their ongoing activation in this disease is mediated, in part, <it>via </it>IgE in the absence of antigen. In this study we have examined whether IgE alone enhances human lung mast cell (HLMC) survival.</p> <p>Methods</p> <p>Purified HLMC were cultured for 4 weeks and survival assays then performed over 10 days following cytokine withdrawal in the presence or absence of human myeloma IgE. Quantitative real time RT-PCR was carried out to examine IL-6 mRNA expression and IL-6 protein was measured in HLMC supernatants by ELISA.</p> <p>Results</p> <p>IgE alone promoted the survival of HLMC in a dose-dependent manner following cytokine withdrawal. IgE-induced survival was eliminated with the addition of neutralising anti-IL-6 antibody but not by the addition of neutralising anti-stem cell factor. IgE sensitisation initiated profound upregulation of IL-6 mRNA in HLMC, and IL-6 concentrations were also raised in the culture supernatants of IgE-exposed cells.</p> <p>Conclusion</p> <p>These data taken together suggest that IgE in the absence of antigen promotes HLMC survival through the autocrine production of IL-6. This provides a further mechanism through which IL-6 and IgE contribute to the pathogenesis of asthma, and through which anti-IgE therapy might achieve its therapeutic effect.</p> http://www.biomedcentral.com/1471-2172/9/2
collection DOAJ
language English
format Article
sources DOAJ
author Cockerill Sarah
Cruse Glenn
Bradding Peter
spellingShingle Cockerill Sarah
Cruse Glenn
Bradding Peter
IgE alone promotes human lung mast cell survival through the autocrine production of IL-6
BMC Immunology
author_facet Cockerill Sarah
Cruse Glenn
Bradding Peter
author_sort Cockerill Sarah
title IgE alone promotes human lung mast cell survival through the autocrine production of IL-6
title_short IgE alone promotes human lung mast cell survival through the autocrine production of IL-6
title_full IgE alone promotes human lung mast cell survival through the autocrine production of IL-6
title_fullStr IgE alone promotes human lung mast cell survival through the autocrine production of IL-6
title_full_unstemmed IgE alone promotes human lung mast cell survival through the autocrine production of IL-6
title_sort ige alone promotes human lung mast cell survival through the autocrine production of il-6
publisher BMC
series BMC Immunology
issn 1471-2172
publishDate 2008-01-01
description <p>Abstract</p> <p>Background</p> <p>Mast cells play a key role in asthma and recent evidence indicates that their ongoing activation in this disease is mediated, in part, <it>via </it>IgE in the absence of antigen. In this study we have examined whether IgE alone enhances human lung mast cell (HLMC) survival.</p> <p>Methods</p> <p>Purified HLMC were cultured for 4 weeks and survival assays then performed over 10 days following cytokine withdrawal in the presence or absence of human myeloma IgE. Quantitative real time RT-PCR was carried out to examine IL-6 mRNA expression and IL-6 protein was measured in HLMC supernatants by ELISA.</p> <p>Results</p> <p>IgE alone promoted the survival of HLMC in a dose-dependent manner following cytokine withdrawal. IgE-induced survival was eliminated with the addition of neutralising anti-IL-6 antibody but not by the addition of neutralising anti-stem cell factor. IgE sensitisation initiated profound upregulation of IL-6 mRNA in HLMC, and IL-6 concentrations were also raised in the culture supernatants of IgE-exposed cells.</p> <p>Conclusion</p> <p>These data taken together suggest that IgE in the absence of antigen promotes HLMC survival through the autocrine production of IL-6. This provides a further mechanism through which IL-6 and IgE contribute to the pathogenesis of asthma, and through which anti-IgE therapy might achieve its therapeutic effect.</p>
url http://www.biomedcentral.com/1471-2172/9/2
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AT cruseglenn igealonepromoteshumanlungmastcellsurvivalthroughtheautocrineproductionofil6
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