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Many investigators now accept that chronic inflammation of the bronchial mucosa plays a fundamental role in the pathogenesis of asthma. This inflammation resembles a cell-mediated reaction in which selective release of cytokines, principally by activated T lymphocytes but also by other cells, brings about the accumulation and activation of granulocytes. Of the granulocytes, eosinophils are particularly implicated in causing the bronchial mucosal damage that is thought to underlie the clinical manifestations of asthma. Glucocorticoids, which inhibit T lymphocyte activation and cytokine release, currently form the mainstay of asthma therapy. However, many patients do not respond adequately to this therapy and consequently suffer from severe disease. Novel therapies for asthma, such as cytokine antagonists and monoclonal antibodies directed against pro-inflammatory effector cells, show great promise for the future. These agents are based on a knowledge of disease pathogenesis and are particularly directed against the T cell/cytokine/eosinophil interactions evident in the disease. They are urgently needed for those patients whose response to glucocorticoids is inadequate.