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


CONCLUSIONS
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.
Stanciu
Luminita A
LA
Department of Respiratory Medicine, National Heart and Lung Institute, Wright Fleming Institute for Infection and Immunity, Imperial College London, Norfolk Place, London, UK. l.stanciu@imperial.ac.uk
Roberts
Kevan
K
Papadopoulos
Nikolaos G
NG
Cho
Sang-Heon
SH
Holgate
Stephen T
ST
Coyle
Anthony J
AJ
Johnston
Sebastian L
SL
D000328:Adult; D001249:Asthma / Q000145:classification / Q000276:immunology* / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology*; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D039041:Integrin alpha4beta1 / Q000276:immunology*; D018793:Interleukin-13 / Q000276:immunology*; D015847:Interleukin-4 / Q000276:immunology*; D015848:Interleukin-5 / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology; D016169:Lymphocyte Function-Associated Antigen-1 / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D039041:Integrin alpha4beta1; D018793:Interleukin-13; D015848:Interleukin-5; D016169:Lymphocyte Function-Associated Antigen-1; D015847:Interleukin-4