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 Omenaas et 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 . . . [Full text of this article]