RT Journal Article
SR Electronic
T1 The profile of dendritic cell and T cell response is related to the viral trigger in children with severe asthma exacerbation
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 3112
VO 40
IS Suppl 56
A1 Clémence Mordacq
A1 Antoine Deschildre
A1 Isabelle Tillie-Leblond
A1 Anny Dewilde
A1 Muriel Pichavant
A1 Caroline Thumerelle
A1 David Romero
A1 Philippe Gosset
YR 2012
UL http://erj.ersjournals.com/content/40/Suppl_56/3112.abstract
AB Viral infection are associated with asthma exacerbations (AE). Activation of dendritic cells (DC) plays a key role in the response to virus and drives the activation and polarization of T cells. Mobilization of Pattern Recognition Receptor (PRR): Toll Like Receptor (TLR3), RNA helicases (RIG-I, MDA-5) are involved. Our purpose was to analyze expression and function of the PRR in DC and to corroborate this with the presence of virus and the T cell response.Methods: 54 allergic asthmatic children (6-15 y) included during hospitalization for severe AE. Virus identified on nasal secretions by RT-PCR. T cell response determined in blood and induced sputum at the inclusion and in the stable state, 8 weeks later. Mononuclear cells (MNC) stimulated in vitro with poly(IC) and liposomes containing poly(IC) and levels of IL-4, IFN-g, IL-17A measured. Expression of markers of maturation (CD80, CD86) and PRR studied in circulating DC by flow cytometry.Results: Virus were indentified in 60 % (Rhinovirus: 82 %). A Th1 and Th17 (IFNg, IL17A) response was observed in the airways and the blood from the infected patients (V+) during exacerbation whereas a Th2 (IL-4) response prevailed in non-infected patients (V-). The stimulation of MNC induced a Th2 and Th17 response for V+ at inclusion, but Th1 in V-. A defect in RNA helicases expression by blood DC was observed in V+ at inclusion, while the expression of the markers of maturation did not differ among both groups.Conclusion: Viral infection modifies the T cell response during AE and is associated with a defect of RNA-helicase expression in DC. This could contribute to describe new mechanisms in the virus induced AE.