Gene–environment interactions in asthma and allergy: the end of the beginning?

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Purpose of review

The pathogenesis of asthma and allergy typically involves not only distinct genetic and environmental factors, but also interactions between the two. Innate-immunity genes [particularly CD14, toll-like receptor (TLR)4 and TLR2, the critical mediators of responses to bacteria in the extracellular space] play a prominent role in gene–environment interactions relevant to asthma-related phenotypes because the interaction between microbial load and the innate-immune system is a critical determinant of both immune function and allergy/asthma susceptibility. This review presents recent findings illustrating the role of gene–environment interactions in asthma/allergy susceptibility.

Recent findings

Population studies have extended our understanding of the role of CD14 and innate-immune genes in the interplay between genetic variants and the environment, highlighting the complexity of these interactions and their significant influence on susceptibility to asthma and allergy.


Gene–environment interactions have become a leitmotiv in asthma and allergy genetics, especially over the last 3 years. The next challenge awaiting asthma and allergy geneticists will be to define the extent to which the search for gene–environment interactions can be successfully integrated with hypothesis-generating, genome-wide approaches aimed at the identification of genetic variants involved in the pathogenesis of complex-lung diseases.

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