Objective: It has become increasingly clear that the mechanisms by which an allergic immune response is generated are complex and may begin even before a baby is born. Genetic, environmental, nutritional, and immunologic factors acting during pregnancy all play a role in determining whether or not a baby is born with a propensity to develop allergic sensitization and subsequent allergic disease. The objective of the research described in this article is to determine whether manipulation of any or all of these could lead to prevention of disease.
Data sources: The database used was Medline up to and including 1997. The Conference Proceedings of the XVth World Congress of Asthmology in Montpellier 1996 are quoted. Many of the research hypotheses are generated from work performed in our own laboratories.
Study selection: The criteria used to select studies for review centered around a necessity for the data to have been collected in very early life with, if possible, a follow-up period to determine disease progression, or for the data to have been collected during pregnancy to elucidate primary mechanisms.
Results: It has been shown that a fetus is able to mount a proliferative response to a common allergic trigger (beta-lactoglobulin, house dust mite, etc) as early as 22 weeks of pregnancy. Maternal exposure to allergens influences her own IgG production which modulates the allergen exposure of the fetus resulting in either primary sensitization of T cells or "tolerance" to the allergen. Atopic mothers create a more Th2-orientated environment for the developing fetus than non-atopic mothers.
Conclusions: Manipulation of the maternal immune response during pregnancy, either by altering her environment or controlling her allergic reactions, may be a method of preventing the development of allergic disease in infants.