<P>Summary</P><P>Natural killer T (NK T) cells have been shown to play an essential role in the development of allergen-induced airway hyperresponsiveness (AHR) and/or airway inflammation in mouse models of acute asthma. Recently, NK...
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https://www.riss.kr/link?id=A107575064
Koh, Y.-I. ; Shim, J.-U. ; Lee, J.-H. ; Chung, I.-J. ; Min, J.-J. ; Rhee, J. H. ; Lee, H. C. ; Chung, D. H. ; Wi, J.-O.
2010
-
SCI,SCIE,SCOPUS
학술저널
159-170(12쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
<P>Summary</P><P>Natural killer T (NK T) cells have been shown to play an essential role in the development of allergen-induced airway hyperresponsiveness (AHR) and/or airway inflammation in mouse models of acute asthma. Recently, NK...
<P>Summary</P><P>Natural killer T (NK T) cells have been shown to play an essential role in the development of allergen-induced airway hyperresponsiveness (AHR) and/or airway inflammation in mouse models of acute asthma. Recently, NK T cells have been reported to be required for the development of AHR in a virus induced chronic asthma model. We investigated whether NK T cells were required for the development of allergen-induced AHR, airway inflammation and airway remodelling in a mouse model of chronic asthma. CD1d<SUP>−/−</SUP> mice that lack NK T cells were used for the experiments. In the chronic model, AHR, eosinophilic inflammation, remodelling characteristics including mucus metaplasia, subepithelial fibrosis and increased mass of the airway smooth muscle, T helper type 2 (Th2) immune response and immunoglobulin (Ig)E production were equally increased in both CD1d<SUP>−/−</SUP> mice and wild-type mice. However, in the acute model, AHR, eosinophilic inflammation, Th2 immune response and IgE production were significantly decreased in the CD1d<SUP>−/−</SUP> mice compared to wild-type. CD1d-dependent NK T cells may not be required for the development of allergen-induced AHR, eosinophilic airway inflammation and airway remodelling in chronic asthma model, although they play a role in the development of AHR and eosinophilic inflammation in acute asthma model.</P>