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Joshua A. Boyce and K. Frank Austen

J.A.B. and K.F.A. are at Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.

CORRESPONDENCE K.F.A.: fausten{at}rics.bwh.harvard.edu OR J.A.B.: Jboyce{at}rics.bwh.harvard.edu

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.

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