S-Space College of Medicine/School of Medicine (의과대학/대학원) Immunology (면역학전공) Journal Papers (저널논문_면역학전공)
IL-4 increases type 2, but not type 1, cytokine production in CD8+ T cells from mild atopic asthmatics
- Stanciu, L. A.; Roberts, K.; Papadopoulos, N. G.; Cho, S. H.; Holgate, S. T.; Coyle, A. J.; Johnston, S. L.
- Issue Date
- BioMed Central
- Respir Res. 2005 Jul 7;6:67.
- Adult; Asthma/classification/*immunology/pathology; CD8-Positive T-Lymphocytes/*immunology; Cells, Cultured; Female; Humans; Integrin alpha4beta1/*immunology; Interleukin-13/*immunology; Interleukin-4/*immunology; Interleukin-5/*immunology; Lymphocyte Activation/immunology; Lymphocyte Function-Associated Antigen-1/*immunology; Male; Middle Aged; Th1 Cells/immunology; Th2 Cells/immunology
- 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.
- 1465-993X (Electronic)