The role of IgE in eosinophil recruitment and bronchial hyperresponsiveness
has been extensively studied with murine models of inflammation. Many inve
stigators using various knockout models have clearly shown that both IgE-de
pendent and -independent pathways play a role in eosinophil recruitment and
bronchial hyperresponsiveness after allergen challenge, illustrating the c
omplexity of airways inflammation. The expression of this response is likel
y to involve many interacting pathways, and it will be a considerable chall
enge to determine key points within these pathways that will yield novel ta
rgets for future therapeutic strategies.