Recent evidence points to the recruitment of T(H)2 cells, phenotype T lymphocytes, their activation, and the generation of T(H)2 cytokines, particularly IL-4 and IL-5, in both peripheral blood and bronchial mucosa of asthmatic patients, leading to local tissue eosinophilia and IgE-dependent mast-cell activation. Activation of T(H)2 T lymphocytes appears to be specific for asthma (as opposed to airway obstructive disease) and was shown to correlate with asthma severity as evidenced by the inverse correlation between CD25(+)/CD4(+) cells and peak expiratory flow rates. These findings support the fundamental importance of T-lymphocyte responses in bronchial asthma and delineate potential therapeutic strategies, such as broad-based immunosuppression versus a more selective approach targeted against CD4(+) T lymphocytes. The high efficacy of topical treatments (ie, inhalation) supports the notion that changes that are detectable in peripheral blood merely reflect a "spill-over" of local T-lymphocyte responses in the target organ. Conversely, the multiple systemic manifestations of allergy (such as allergic rhinitis and atopic dermatitis in atopic patients) support systemic therapeutic approaches.