The T cell hypothesis of asthma, particularly chronic asthma, is based around the concept that the disease is driven and maintained by the persistence of a specialized subset of chronically activated T memory cells sensitized against an array of allergenic, occupational or viral antigens which home to the lung after appropriate antigen exposure or viral infection. Allergens induce a CD⁴⁺ T helper (Th) cell response, whereas viruses recognize CD⁸⁺ T cytotoxic (Tc) cells. In the asthmatic airways there appears to be both CD⁴⁺ and CD⁸⁺ cells with a type 2 cytokine phenotype (i.e. Th2 and Tc2 type). These cells produce: interleukin (IL)‐5, IL‐3 and granulocyte macrophage colony‐stimulating factor, which recruit, mobilize and activate eosinophils for subsequent mucosal tissue damage; and IL‐4, an essential co‐factor for local or generalized IgE production. This in turn leads to eosinophilic desquamative bronchitis, with epithelial shedding, mucus hypersecretion and bronchial smooth muscle contraction. Thus, although the eosinophil is largely responsible for airway symptoms, its function appears to be under T cell control. Support for this hypothesis includes: the observations that activated T cells and their products can be identified in biopsies from the major variants of the disease (atopic, non‐atopic [intrinsic] and occupational asthma); the co‐localization of mRNA for type 2 cytokines to CD⁴⁺ and CD⁸⁺ cells in atopic and non‐atopic asthma; the presence of chronically activated cytokine‐producing T cells in corticosteroid‐resistant asthma; the association of disease severity with type 2 cytokines, especially IL‐5; and the efficacy of cyclosporin A in chronic steroid‐dependent disease. Inhibitors and/or antagonists directed against more precise T cell‐associated molecular targets hold promise for the future treatment of chronic asthma.