Abstract
The recognition that a special type of inflammation throughout the conducting airways is fundamental to their disordered function in asthma linked to bronchial hyperresponsiveness (BHR) and variable airflow obstruction has provided the basis for modern treatment with controller drugs, such as inhaled corticosteroid and leukotriene receptor antagonists. The nature of this inflammation has been the focus of intense research in the hope of discovering selective pathways amenable to therapeutic intervention. Because a high proportion of asthma is associated with atopy, it is proposed that in genetically susceptible individuals, exposure to aeroallergens leads to their processing by epithelial dendritic cells (DCs) to generate selective peptides that, when presented to the T-cell receptor (TCR) in the context of MHC class II molecules, lead to cell proliferation and coordinate expression of a cluster of cytokine genes on chromosome 5q31-34 that encode IL-3, IL-4, IL-5, IL-9, IL-13, and GM-CSF. This response, designated TH2-like, is to be differentiated from alternative T-cell responses involving production of IL-2, TNF, and IFN-? (TH1); IL-10 (T reg); and TGF-? (TH3). TH2 cytokines are fundamental to the recruitment, differentiation, and priming of the principal effector leukocytes of asthmatic inflammation: mast cells, eosinophils, basophils, and monocytes-macrophages.
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