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In this issue of Thorax there are two articles which add to the observations on an inverse link between mycobacterial exposure and atopic disorder, and to the larger story that certain microbial exposures in early childhood may play a key part in limiting immune dysregulation. Von Mutius and colleagues report increasing tuberculosis notification rates associated with a stepwise decrease in symptoms of asthma and rhinoconjunctivitis in an international ecological study,1 while Omenaaset al found no relationship between IgE levels and tuberculin responses in Norwegian adults vaccinated with BCG at 14 years of age.2
One potential explanation for the promotion of clinical tolerance to allergens by certain microbial exposures may be framed within two related immunological concepts. Firstly, adaptive immune responses may be broadly categorised into two antagonistic subtypes (Th1 and Th2), each with its own set of molecular mediators or cytokines.3-5 Secondly, the type of T helper (Th) adaptive response to one antigen may influence the type of Th response to a quite independent antigen through modification of the cytokine profile of the immune milieu.6-8
In atopy there is over-reactivity of Th2 immune mechanisms involving the cytokines interleukin (IL)-4, IL-5 and IL-3, which leads to IgE production and eosinophilic mucosal inflammation in response to many antigens. Atopic or allergic responses to inhaled antigen or allergen such as those from house dust particles are a potent factor in the causation of asthma.6 9 10 Such vigorous Th2 immune responses are naturally seen in certain helminthic infections when they provide an important element of protective immunity.11-13What then is their origin, in dysregulated form, in atopy?
Heterogeneous genetic factors are important because genetic variants at a number of chromosomal locations are linked to high IgE levels or asthma.14 Variants in the Th2 cytokine signalling …
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