@article {616,
	title = {IL-4 increases type 2, but not type 1, cytokine production in CD8+ T cells from mild atopic asthmatics},
	journal = {Respir Res},
	volume = {6},
	year = {2005},
	pages = {67},
	type = {Journal Article},
	abstract = {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.|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.|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.|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.},
	keywords = {Adult Asthma CD8-Positive T-Lymphocytes Cells, Cultured Female Humans Integrin alpha4beta1 Interleukin-13 Interleukin-4 Interleukin-5 Lymphocyte Activation Lymphocyte Function-Associated Antigen-1 Male Middle Aged Th1 Cells Th2 Cells},
	issn = {1465-993X},
	doi = {10.1186/1465-9921-6-67},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/16001979},
	author = {Stanciu, L. A. and Roberts, K. and Papadopoulos, N. G. and Cho, S. H. and Holgate, S. T. and Coyle, A. J. and Johnston, S. L.}
}
