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The Editor takes a closer look at some of this month's articles

Central to ideas about the pathogenesis of asthma is the concept of allergen-stimulated Th2 cells and mast cells orchestrating the inflammatory process in the airways. However, together with the realization that IgE-mediated allergic reactions are closely associated with asthma and that airway challenge with allergen can mimic some of the features of asthma, came the awareness that in a significant proportion of asthmatics there is no evidence of specific IgE to common aeroallergens (the patient is non-atopic), or an environmental cause for their symptoms. The term intrinsic asthma was coined to describe this phenotype, which is more commonly seen in adult asthma and is often characterized by florid eosinophilic airway inflammation [1]. In some situations, particularly occupational asthma, an allergen can be identified that appears to be working through a non-IgE-mediated mechanism, but in the majority of non-atopic asthmatics the cause is not known. Clinical and Experimental Allergy therefore invited a number of eminent investigators to speculate on the aetiology of intrinsic asthma. The first paper in this mini-series (Holt et al., pp. 807–811) presents the idea that infections, particularly viral infections in early childhood, developmentally predispose people to airway disease, which manifests itself when another airway irritant such as smoking, pollution or another infection occurs; a stimulating idea that sets the bar high for the rest of our authors on this topic.