Atopy is defined by an individual propensity to develop IgE-dependent react
ions against environmental allergens. It could be now defined by a propensi
ty to develop a Th2 response against such allergens, which takes into accou
nt not only the IgE production but also the eosinophil activation and the p
ivotal role of T lymphocytes in this process.
A number of factors are determinants of atopy: some of them precede birth,
such as generic factors and some peculiarities of the immune system during
pregnancy, in relation to maternal atopy, to in utero allergen exposure or
to pregnancy itself: After birth, car pollution could modify the response t
o allergens by enhancing the IgE production. Food habits, by favoring intak
e of omega-6 polyunsaturated fat acids contained in some vegetal fat instea
d of omega-3 polyunsaturated acids from fish, could facilitate IgE dependen
t sensitization. Viral infections could, depending on their nature and thei
r circumstances of occurrence protect from atopy inversely induce some sens
itizations. Finally the degree of exposure to allergens themselves is propo
rtional to the probability of sensitization. Together, these determinants o
f atopy could account for the higher prevalence of atopy in developed count
ries.
The clinical expression of atopy varies during life from atopic dermatitis
to rhinitis and asthma. Infancy is the time for dermatitis and sensitizatio
n to food allergens. Sensitization to airborne allergens occurs thereafter.
Asthma, sometimes introduced by one or several bronchiolitis episodes foll
ows to dermatitis or cart be associated to it. Rhinitis appears in children
or young adults. Seasonal, it is due to pollens and is rarely associated w
ith asthma. In contrast, perennial, it is due to indoor allergens and leads
to bronchial hyperreactivity and asthma.