<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Stanciu, L. A.</style></author><author><style face="normal" font="default" size="100%">Roberts, K.</style></author><author><style face="normal" font="default" size="100%">Papadopoulos, N. G.</style></author><author><style face="normal" font="default" size="100%">Cho, S. H.</style></author><author><style face="normal" font="default" size="100%">Holgate, S. T.</style></author><author><style face="normal" font="default" size="100%">Coyle, A. J.</style></author><author><style face="normal" font="default" size="100%">Johnston, S. L.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">IL-4 increases type 2, but not type 1, cytokine production in CD8+ T cells from mild atopic asthmatics</style></title><secondary-title><style face="normal" font="default" size="100%">Respir Res</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult Asthma CD8-Positive T-Lymphocytes Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">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</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16001979</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">67</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">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.</style></abstract><work-type><style face="normal" font="default" size="100%">Journal Article</style></work-type></record></records></xml>