[Synthesis and modulation of IgE in the newborn infant]

Abstract

The synthesis of IgE class antibodies takes place in plasma cells after activation of B lymphocytes by two different signals. The presence of interleukin-4 (IL-4) in the microenvironment and intimate contact between B and T cells through the CD-40 molecule and its specific ligand (CD-40L) are necessary. Lymphocyte activation also can be induced by mast cells. IgE does not cross the placenta, but fetuses are capable of synthesizing it. We attempted to identify children at high risk of atopy by determining IgE in umbilical cord blood. The system was not entirely satisfactory because many other factors are involved, but it demonstrated that intrauterine sensitization can occur. IgE-mediated allergy is conditioned by the predominance of Th2 lymphocytes (secretors of IL-4, IL-5, and IL-10) over Th1 lymphocytes (secretors of IL-12 and IFN gamma). This imbalance is physiological in the fetus and Th1 stimulation causes miscarriage. At birth, the functional predominance of Th2 continues, probably because of the immaturity of the dendritic antigen-presenting cells. An irregular maturation process takes place in the following months; for instance, while the intestinal mucosa tends towards tolerance and matures more rapidly, the respiratory mucosa tends toward the Th1 response and is slower. It is likely that sensitization during fetal and neonatal life is interesting because it generates type Th2 memory cells that can predispose toward atopic responses in the future.