Complex diseases, including diseases of allergic origin (asthma, rhinitis, dermatitis), tend to cluster in families, suggesting the existence of a genetic predisposition that has been confirmed by the family and twin studies. However, it is difficult to establish a clear Mendelian pattern of inheritance and it is accepted that multiple genes exist which have an additive effect (polygeny) and interact with environmental factors (multifactorial polygenic mechanism) to cause not only the atopic constitution but also the pathology that derives from it. Advances in genetics and molecular biology, through linkage studies in chosen family nuclei and different population groups, are facilitating the location of chromosomal regions related with allergic pathology. The genes situated in these regions are considered candidate genes, and the genes themselves and the functions that they control are studied in relation to allergic disease. Although there are regions and candidate genes distributed throughout the genome, chromosomes 5, 6, 11, and 14 contain genes whose responsibility for susceptibility to atopy, asthma and bronchial hyperreactivity is accepted and whose polymorphisms could be risk factors. The study of these genes and many other candidate genes may clarify some etiopathogenic aspects of diseases of allergic origin and improve their prophylaxis and therapy.
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