[Natural history of atopy]

Atopy is defined by an individual propensity to develop IgE-dependent reactions against environmental allergens. It could be now defined by a propensity to develop a Th2 response against such allergens, which takes into account not only the IgE production but also the eosinophil activation and the pivotal role of T lymphocytes in this process. A number of factors are determinants of atopy: some of them precede birth, such as genetic 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 to allergens by enhancing the IgE production. Food habits, by favoring intake of omega-6 polyunsaturated fat acids contained in some vegetal fat instead of omega-3 polyunsaturated acids from fish, could facilitate IgE dependent sensitization. Viral infections could, depending on their nature and their circumstances of occurrence protect from atopy inversely induce some sensitizations. Finally the degree of exposure to allergens themselves is proportional to the probability of sensitization. Together, these determinants of atopy could account for the higher prevalence of atopy in developed countries. The clinical expression of atopy varies during life from atopic dermatitis to rhinitis and asthma. Infancy is the time for dermatitis and sensitization to food allergens. Sensitization to airborne allergens occurs thereafter. Asthma, sometimes introduced by one or several bronchiolitis episodes follows to dermatitis or can be associated to it. Rhinitis appears in children or young adults. Seasonal, it is due to pollens and is rarely associated with asthma. In contrast, perennial, it is due to indoor allergens and leads to bronchial hyperreactivity and asthma.