Basic of Sensitization in Atopic Allergy

Basic of Sensitization in Atopic Allergy
During the first year of life, allergic sensitization occurs readily via the intestinal tract because the protective immunologic mechanisms are not fully developed.

Breast milk offers passive protection during the vulnerable age but is also a possible route of sensitization.

Overproduction of IgE is characteristics of atopic allergy. Many healthy children develop IgE antibodies, against egg white for instance, during the first year of life.

These antibodies usually disappears in a few months and are probably a reflection of the normal humoral immunoresponse.

However, in those children who manifest a clinical allergy to egg white, antibodies disappear more slowly. It has been postulated that the function of cells, especially lymphocytes, controlling IgE synthesis is not in balance.

Atopy may be related to deficient or retarded maturation of cells suppressing IgE synthesis.

The protective mechanism of the intestinal mucosa, although their exact nature is not known, prevent sensitization effectively. From animal studies it is known that mice develop antibodies when given cow’s milk protein parenterally.

However, if the animal is fed cow’s milk before the injection, it develops immunotolerence and no antibodies can be detected.

The role of mucosal IgA is vitally important. Quantitative or qualitative deficiencies of IgA enhance the manifestation of circulation antibodies to foreign proteins as well as the formation of immunocomplexes.

If the permeability of the gastrointestinal or respiratory tract is increased for some reason, allergens penetrate the mucous membranes more easily and induce an immunologic response.

The function of the intestinal mucosal barrier is disturbed by infections, dietary habits, ingestions of alcohol and drugs and so fourth.
Basic of Sensitization in Atopic Allergy