Asthma is a spreading condition in Western countries, in most cases in rela
tionship with atopy. Atopy is defined by an individual predisposition to de
velop allergic diseases in response to environmental allergens. The atopic
immune system is characterized by a Th2 deviation determined by genetic and
environmental factors. Among these factors, the role of allergen exposure,
dietary behavior, air pollution and early exposure to microbes is discusse
d. In asthma, a Th2 cell activation is evident but is accompanied by a Tc1
cell activation. These Tc1 cells probably down-regulate Th2 cells, but are
also relevant to the bronchial hyperresponsiveness characterizing asthma. W
e propose that Tc1 activation in asthma could be the link between allergy a
nd bronchial hyperresponsiveness.