No audible wheezing
Open Access
- 20 June 2005
- journal article
- research article
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 201 (12) , 1869-1873
- https://doi.org/10.1084/jem.20050584
Abstract
Mouse models of T helper type 2 (Th2) cell–biased pulmonary inflammation have elucidated mechanisms of sensitization, cell traffic, and induced airway hyperresponsiveness (AHR). Nonetheless, most mice lack intrinsic AHR, a central property of human asthma, and disparities persist regarding the contributions of eosinophils and mast cells and the sensitivity to induced AHR in the commonly used mouse strains. We suggest that these discordances, reflecting methodological and genetic differences, may be informative for understanding heterogeneity of human asthma.Keywords
This publication has 36 references indexed in Scilit:
- Interacting genetic loci cause airway hyperresponsivenessPhysiological Genomics, 2005
- A Critical Role for Eosinophils in Allergic Airways RemodelingScience, 2004
- Defining a Link with Asthma in Mice Congenitally Deficient in EosinophilsScience, 2004
- Intrinsic Defect in T Cell Production of Interleukin (IL)-13 in the Absence of Both IL-5 and Eotaxin Precludes the Development of Eosinophilia and Airways Hyperreactivity in Experimental AsthmaThe Journal of Experimental Medicine, 2002
- Interleukin-13 Induces Tissue Fibrosis by Selectively Stimulating and Activating Transforming Growth Factor β1The Journal of Experimental Medicine, 2001
- Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity.The Journal of Experimental Medicine, 1996
- Quantitative locus analysis of airway hyperresponsiveness in A/J and C57BL/6J miceNature Genetics, 1995
- An interleukin 4 (IL-4) mutant protein inhibits both IL-4 or IL-13-induced human immunoglobulin G4 (IgG4) and IgE synthesis and B cell proliferation: support for a common component shared by IL-4 and IL-13 receptors.The Journal of Experimental Medicine, 1993
- Mast cell activation enhances airway responsiveness to methacholine in the mouse.Journal of Clinical Investigation, 1993
- Predominant TH2-like Bronchoalveolar T-Lymphocyte Population in Atopic AsthmaNew England Journal of Medicine, 1992