It is now well established that a subset of T-cell-derived cytokines (termed Th2 cytokines) programme the timing and characteristics of atopic airway disease including mast-cell sensitization, eosinophil and lymphocyte infiltration and recently mucus secretion. To date, attempts to devise ways to selectively limit the activities of Th2 cytokine-producing cells have been frustrated. However, the recent identification of the molecules which direct the activation and maturation of T cells has led to some successful attempts to block the activities of Th2 cells in models of atopic airway inflammation. Some of the agents with the most potential include antagonists of the T-cell costimulatory molecule CD28, local stimulators of the Thl subset of cytokines such as the BCG vaccine and potentially, antagonists of the eotaxin chemokine receptor and agonists of the T-cell costimulatory molecule CTLA-4. Not only do such agonists and antagonists represent potential new therapies, they could represent a rich hunting ground for those who aim to determine the ways in which atopic airway disease can be diagnosed and understood.