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IL-4 increases type 2, but not type 1, cytokine production in CD8+ T cells from mild atopic asthmatics

Cited 10 time in Web of Science Cited 9 time in Scopus
Authors
Stanciu, L. A.; Roberts, K.; Papadopoulos, N. G.; Cho, S. H.; Holgate, S. T.; Coyle, A. J.; Johnston, S. L.
Issue Date
2005-07-09
Publisher
BioMed Central
Citation
Respir Res. 2005 Jul 7;6:67.
Keywords
AdultAsthma/classification/*immunology/pathologyCD8-Positive T-Lymphocytes/*immunologyCells, CulturedFemaleHumansIntegrin alpha4beta1/*immunologyInterleukin-13/*immunologyInterleukin-4/*immunologyInterleukin-5/*immunologyLymphocyte Activation/immunologyLymphocyte Function-Associated Antigen-1/*immunologyMaleMiddle AgedTh1 Cells/immunologyTh2 Cells/immunology
Abstract
BACKGROUND: Virus infections are the major cause of asthma exacerbations. CD8+ T cells have an important role in antiviral immune responses and animal studies suggest a role for CD8+ T cells in the pathogenesis of virus-induced asthma exacerbations. We have previously shown that the presence of IL-4 during stimulation increases the frequency of IL-5-positive cells and CD30 surface staining in CD8+ T cells from healthy, normal subjects. In this study, we investigated whether excess IL-4 during repeated TCR/CD3 stimulation of CD8+ T cells from atopic asthmatic subjects alters the balance of type 1/type 2 cytokine production in favour of the latter. METHODS: Peripheral blood CD8+ T cells from mild atopic asthmatic subjects were stimulated in vitro with anti-CD3 and IL-2 +/- excess IL-4 and the expression of activation and adhesion molecules and type 1 and type 2 cytokine production were assessed. RESULTS: Surface expression of very late antigen-4 [VLA-4] and LFA-1 was decreased and the production of the type 2 cytokines IL-5 and IL-13 was augmented by the presence of IL-4 during stimulation of CD8+ T cells from mild atopic asthmatics. CONCLUSION: These data suggest that during a respiratory virus infection activated CD8+ T cells from asthmatic subjects may produce excess type 2 cytokines and may contribute to asthma exacerbation by augmenting allergic inflammation.
ISSN
1465-993X (Electronic)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16001979

http://hdl.handle.net/10371/22603
DOI
https://doi.org/10.1186/1465-9921-6-67
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College of Medicine/School of Medicine (의과대학/대학원)Immunology (면역학전공)Journal Papers (저널논문_면역학전공)
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