Leicester Research Archive >
College of Medicine, Biological Sciences and Psychology >
Infection, Immunity and Inflammation, Department of >
Published Articles, Dept. of Infection, Immunity and Inflammation >
Please use this identifier to cite or link to this item:
|Title: ||IgE alone promotes human lung mast cell survival through the autocrine production of IL-6|
|Authors: ||Cruse, Glenn|
|Issue Date: ||23-Jan-2008|
|Publisher: ||BioMed Central Ltd|
|Citation: ||BMC Immunology 2008, 9:2|
|Abstract: ||Background: Mast cells play a key role in asthma and recent evidence indicates that their ongoing
activation in this disease is mediated, in part, via IgE in the absence of antigen. In this study we have
examined whether IgE alone enhances human lung mast cell (HLMC) survival.
Methods: 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.
Results: 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.
Conclusion: 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.|
|DOI Link: ||10.1186/1471-2172-9-2|
|Version: ||Publisher Version|
|Type: ||Journal Article|
|Appears in Collections:||Published Articles, Dept. of Infection, Immunity and Inflammation|
Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.