Abstract
Activated mast cells, eosinophils, and basophils infiltrate the airways
of asthmatics as a result of an overexuberant T helper 2 (Th2) cell
immune response that drives the production of IgE, primes mast cells and
basophils, and promotes tissue eosinophilia and mast cell hyperplasia.
Recent evidence demonstrates that these innate effectors can be
activated outside of this classical Th2 cell paradigm and that they have
additional roles in promoting the development of innate and adaptive
pulmonary inflammation. There is also an appreciation for the role of
airway epithelial cells in orchestrating allergic pulmonary
inflammation. Emerging data from basic research highlight the
involvement of many unique pathways in the inflammation triggered by
complex native allergens and microbes at the airway mucosal surface.
Here, we review the role of effector cells and airway epithelial cells
in augmenting and, at times, bypassing traditional Th2 cell-mediated
allergic inflammation.
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