Abstract

Atopic disorders represent common and debilitating diseases, with a rising incidence over the last 30 y. Almost 30% of the population is affected by a form of atopic disorder. Many study designs have attempted to elucidate the role of genetic and environmental factors in the causation of atopy (Cookson and Moffat, 1999). This task is not simple, as the pathogenesis of atopy is complex, with the likelihood of gene–environment interactions. The relative contribution of genes and environment in the pathogenesis of atopy is not known, but numerous studies have shown that atopy clusters in families. It is likely that many different genes are responsible for an individual's predisposition to allergy and that exposure to certain known and unknown allergens leads to the expression of asthma, eczema, or hay fever. Twin studies have also been useful in estimating the relative importance of genes and environment on atopy, including eczema (Schultz Larsen, 1993;Lichtentstein and Svartengren, 1997; Strachan et al, 2000). Studies based on more than 3000 UK female twins have shown heritability estimates for eczema of 60%, with models being in favor of a combination of additive genes and unique environment (Mikkilineni et al, 2001). Candidate gene approaches for putative atopy genes have already been conducted by many groups in diverse populations, mainly using the family design (Ono, 2000). Many genes appear to have modest effects on the risk of atopy, and using genome-wide scans many chromosomal regions have been linked to the risk of atopy.

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