Immunoregulatory networks in asthma

It is now well established that a subset of T-cell-derived cytokines (terme d Th2 cytokines) programme the timing and characteristics of atopic airway disease including mast-cell sensitization, eosinophil and lymphocyte infilt ration and recently mucus secretion. To date, attempts to devise ways to se lectively limit the activities of Th2 cytokine-producing cells have been fr ustrated. However, the recent identification of the molecules which direct the activation and maturation of T cells has led to some successful attempt s to block the activities of Th2 cells in models of atopic airway inflammat ion. Some of the agents with the most potential include antagonists of the T-cell costimulatory molecule CD28, local stimulators of the Th1 subset of cytokines such as the BCG vaccine and potentially, antagonists of the eotax in chemokine receptor and agonists of the T-cell costimulatory molecule CTL A-4. Not only do such agonists and antagonists represent potential new ther apies, they could represent a rich hunting ground for those who aim to dete rmine the ways in which atopic airway disease can be diagnosed and understo od.