It is now widely accepted that bronchial mucosal inflammation is an important feature of the pathogenesis of asthma. Lymphocytes probably play a role in all inflammatory responses which are antigen driven, since they are the only cells which, through the CD3/antigen receptor complex, directly recognise and respond to processed antigens. Activated T-lymphocytes, through the release of lymphokines, have the capacity to control the amount and nature of inflammatory responses. Increasing evidence is accumulating that activated CD4 T-lymphocytes participate in the inflammatory reaction observed in the asthmatic bronchial mucosa, by secreting lymphokines which attract and activate eosinophils and mast cells. CD4 T-lymphocytes may be a potentially important target for glucocorticoid therapy in asthma. Further characterisation of the functional properties of these cells might allow a definition of asthma in terms of functional abnormalities at the cellular level, and may uncover variability in asthma pathogenesis according to its aetiology.