Interleukin-5 and eosinophils induce airway damage and bronchial hyperreactivity during allergic airway inflammation in BALB/c mice
Author:
Affiliation:
1. Cellular Signal Transduction Laboratory, Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University; Canberra Australian Capital Territory Australia
Publisher
Wiley
Subject
Cell Biology,Immunology,Immunology and Allergy
Link
http://www.nature.com/articles/icb199743.pdf
Reference8 articles.
1. Immunological aspects of allergic asthma;Bochner;Annu. Rev. Immunol.,1994
2. Cellular and molecular mechanisms involved in the regulation of eosinophil trafficking in vivo;Hogan;Med. Res. Rev.,1996
3. Interleukin-5 deficiency abolishes eosinophilia. Airways hyperreactivity und lung damage in a mouse asthma model;Foster;J. Exp. Med.,1996
4. InterleLikin-4. but not inlerleukin-5 or eosinophils, is required in a murine model of acute airways hyperreactivity;Corry;J. Exp. Med.,1996
5. Eosinophil recruitment into the respiratory epithelium following antigenic challenge in hyper-IgE mice is accompanied by Interleukin 5-dependent bronchial hyperresponsiveness;Eum;Proc. Natl Acad. Sci. USA,1995
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