I am atopic, but why don't I develop allergy? the association between atopy and clinical expression of allergic disease

Abstract

SummaryAlthough there is a close association between the atopic status of an individual and the development of allergic disease, this relationship is not straightforward because different individuals with similar atopic characteristics can present either with clinical manifestations of different allergic conditions (including asthma, allergic rhinitis, atopic dermatitis and food allergy) or even with no allergic disease. Evidence suggests that the atopic status of an individual is influenced by both genetic and environmental factors, and that defects in target organs and involvement of co‐triggers may additionally be required for the development of specific allergic phenotypes. Genetic linkage studies, employing specific polymorphism screening techniques, have demonstrated that allergic disease is linked to a number of genes and that each gene assumes a variable role in different individuals. This suggests that no single gene is important, but that interaction between several genes and environmental factors is likely to determine the allergic phenotype. More recent studies, nevertheless, have suggested that certain genes may play a more predominant role in the clinical expression of a specific phenotype. In this context, the ADAM‐33 gene appears likely to play an important role in asthma while the serine protease inhibitor Kazal‐type 5 (SPINK5) gene may influence the clinical expression of atopic dermatitis. In view of the biological role of lympho‐epithelial Kazal‐type‐related inhibitor, the protein encoded by SPINK, we hypothesize that SPINK5 may be associated with epithelial defence by lowering its ability to resist allergen penetration.