Asthma is largely an inflammatory disease, with the development of T cell mediated inflammation in the lung following exposure to allergen or other precipitating factors. Currently, the major therapies for this disease are directed either at relief of bronchoconstriction (ie beta-agonists) or are non-specific immunomodulators (ie, corticosteroids). While much attention has been paid to factors that regulate the initiation of an inflammatory response, chronic inflammation may also be due to defects in regulatory mechanisms that limit or terminate immune responses. In this review, we explore the elements controlling both the recruitment of T cells to the lung and their function. Possibilities for future therapeutic intervention are highlighted.