Open AccessSoluble mediators derived from bronchial epithelium are able to drive Th2 differentiation in the context of rhinovirus infection
Author(s) -
Makrinioti Heidi,
Walton Ross,
Papadopoulos Nikolaos,
Edwards Michael,
Telcian Aurica,
Cousins David,
Wanke Kerstin,
Stanciu Luminita,
Akdis Mubeccel,
Megremis Spyridon,
Akdis Cezmi,
Johnston Sebastian
Publication year - 2013
Publication title -
clinical and translational allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.979
H-Index - 37
ISSN - 2045-7022
DOI - 10.1186/2045-7022-3-s1-o1
Subject(s) - rhinovirus , immunology , context (archaeology) , foxp3 , medicine , gata3 , proinflammatory cytokine , virus , biology , inflammation , immune system , paleontology , biochemistry , gene , transcription factor
The majority of acute asthma exacerbations follow upper respiratory infections, and most are rhinovirus induced. The pathways by which a rhinovirus infection may lead to asthma development are still under scrutiny, but the role of bronchial epithelium in driving this mechanism has been considered of great importance. It has been shown that the epithelial derived cytokines IL25, IL33 and TSLP are upregulated in bronchial asthma and could be further induced by virus infection. We hypothesise that such cytokines might influence Th2 cell differentiation in the context of rhinovirus infection.