The mast cell, by virtue of its capacity to release a wide range of pro-inflammatory mediators, its abundant expression of the high-affinity receptor for immunoglobulin E and its strategic location in proximity to blood vessels, mucosal surfaces and smooth muscle, had long been considered as the central effector cell in asthma and other allergic diseases. In recent years there has been a tendency for less importance to be attached to this cell as a central effector in asthma. New findings, however, have led to a resurgence of interest in the mast cell and supported a reevaluation of its role. In particular the discovery that mast cells are a potential source of cytokines has suggested new ways in which mast cell activation could also participate in more persistent and even chronic inflammatory responses which we know are central to the pathophysiology of asthma. This review will address: 1) the main aspects of mast cell biology which are relevant to asthma with particular reference to mediators produced and their biological functions; 2) the evidence implicating the mast cell as an effector cell in both the immediate and delayed airway responses to allergen exposure; 3) how acknowledgement that mast cells act as a source of cytokines permits speculation on their involvement in the chronic inflammatory response of asthma.