The main function of the respiratory tract is to provide a large surface area of thin epithelium for gas exchange. At the same time, this exposed surface and the conducting airways have to be defended against airborne irritants and infectious agents. The principal defence is the barrier formed by airway mucus and the mucociliary escalator. Agents which penetrate the initial defences may be destroyed by phagocytic cells, and may initiate an immune response. Respiratory allergy results when airborne allergens penetrate these defences and elicit and unhelpful immunological response. The nature of the airway immune response depends on the nature of the allergen, the antigen-processing pathway, and the microenvironment which dictates the phenotype of available T lymphocytes. Most allergens elicit IgE antibodies which then bind to mast cells and, when cross-linked, the mast cell releases inflammatory mediators which cause bronchospasm and mucus formation. Some chemical allergens appear able to trigger this pathway without involving IgE. In both cases, other inflammatory cells, especially eosinophils, are then recruited. These cells appear to be responsible for the epithelial damage and increased airways reactivity that characterise asthma. Similar histological patterns are found in atopic asthma, non-atopic asthma, occupational asthma due to low molecular weight chemicals and even in the reactive airways dysfunction syndrome (RADS)/irritant-induced asthma syndrome. Allergic airway inflammation and clinical asthma appear to be common histological and clinical consequences of a variety of specific and non-specific insults to the airways epithelium, airways mast cells and airways T lymphocytes.