Asthma is a complex disease associated with bronchial hyperreactivity and a
topy, making asthma a disease with a phenotype that has been clinically dif
ficult to define. Despite intense research, prevalence of asthma remain rel
atively high. The key reason for the high prevalence and morbility is that
the fundamental mechanisms predisposing individuals to the development of a
sthma are not understood. Familial aggregation observed in this pathology h
as prompted for the search of an involved genetic component. This task is d
ifficult due to the complex nature of asthma. A universally accepted defini
tion for this disease is not available, clinical expression can be modulate
d by environmental factors, and inheritance does not follow a clear Mendeli
an pattern. Establishment of more precise clinical and laboratory criteria
has improved the design and interpretation, of genetic studies. Twin analys
is and segregation studies have demonstrated an important genetic component
with a probably multifactorial pattern, of inheritance. "Sib pair" studies
and familial segregation. analyses have shown linkage between some chromos
omal regions and asthma, including chromosome 5, 6, 7, 11 and 14. The searc
h for major genes in, these chromosomal segments has been focused on loci i
nvolved in the allergic process. Among these, the loci for IL-9 and IL-13 i
n chromosome 5 seem to play an important role in the pathogenesis of asthma
. Understanding the fundamental gene-environmental interactions in the deve
lopment of asthma should lead to earlier identification of susceptible indi
viduals and more effective approaches for disease prevention.