At one time, it seemed likely that new treatments for asthma would be developed from targeting specific steps in an increasingly refined model of the immunopathogenesis of the disease. In broad terms, this conceptual model proposes that allergic sensitization results from presentation of an innocuous inhaled antigen by an antigen-presenting cell (APC), most likely a dendritic cell, to a “T-helper type 0” CD4+ lymphocyte under conditions favoring differentiation along the T-helper type 2 (Th2) pathway. Repeated exposure to the same antigen then promotes expansion of sensitized Th2 cells, and their products, especially interleukin (IL)-3, IL-4, IL-5, IL-9, and IL-13, directly or indirectly change the population and function of immigrant and structural cells in the airways. The changes include attraction and differentiation of mast cell precursors, proliferation, attraction, and activation of eosinophils, and IgE production by B cells. Possible changes induced by repeated release of Th2 cytokines also include the elements of “airway remodeling”: vascular neogenesis, proliferation of bronchial smooth-muscle cells, hyperplasia of mucus-secreting cells, and alterations in the extracellular matrix, including deposition of collagen beneath the basement membrane.1 Again, it is not known whether these effects result from the indirect action of Th2 cytokines—through the action of mediators released from other cells attracted and/or activated, such as eosinophils—or from the direct actions of Th2 cytokines on the structural cells themselves.