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

Curr Opin Allergy Clin Immunol. 2010 Apr;10(2):145-8. doi: 10.1097/ACI.0b013e32833653d7.

Abstract

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.

Summary: 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.

Keywords: Gene-environment interactions; allergy; asthma; genome-wide association studies; innate immunity.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Asthma / epidemiology
  • Asthma / genetics*
  • Asthma / immunology*
  • Disease Susceptibility
  • Environmental Exposure / adverse effects*
  • Host-Pathogen Interactions
  • Humans
  • Hypersensitivity / epidemiology
  • Hypersensitivity / genetics*
  • Hypersensitivity / immunology*
  • Lipopolysaccharide Receptors / immunology
  • Toll-Like Receptor 2 / immunology
  • Toll-Like Receptor 4 / immunology

Substances

  • Lipopolysaccharide Receptors
  • TLR2 protein, human
  • TLR4 protein, human
  • Toll-Like Receptor 2
  • Toll-Like Receptor 4