Although T cells act as a driving force in the asthmatic response, the IgE-mast cell interaction is a central component, as it is for all immediate-type hypersensitivity responses. Therefore, understanding the production of IgE in the fetus provides a key for not only elucidating asthma development in children, but also in exploring the maternal influence on fetal and neonatal sensitization to allergens.
Several studies indicate that increased cord blood levels of IgE are associated with an increased risk of atopy or asthma (Croner and Kjellman 1990; Edenharter et al. 1998; Halonen et al. 1992; Hansen et al. 1992; Hide et al. 1991; Kjellman and Croner 1984; Michel et al. 1980; Ruiz et al. 1991). Other studies do not bear out this association (Hide et al. 1991; Martinez et al. 1995). However, a general belief is that an early and inappropriate immune response can develop toward allergens and that young children with asthma or allergic rhinitis have higher than normal levels of antibodies to inhaled allergens (Okahata et al. 1990). The evidence that fetal B cells are capable of isotype switching supports this idea (Punnonen et al. 1993; Punnonen and de Vries 1994). Furthermore, production of IgM, IgG subclasses, and IgE response to CD40 ligation and cytokines from T cells is similar in neonatal B cells and antigenically naïve adult B cells (Briere et al. 1994; Servet-Delprat et al. 1996), indicating equivalent maturational states of these cell types. However, T cell-dependent isotype switching and immunoglobulin production is limited in a fetus in that it has been documented only for certain pathogens such as in toxoplasmosis; congenital infections such as varicella zoster virus do not induce specific immunoglobulin by birth or early childhood (Paryani and Arvin 1986; Pinon et al. 1990).
Even if the capacity to respond to antigen exists in fetuses and newborns, the immune response to innocuous antigen could be due to developmental issues. One line of reasoning states that altered fetal and neonatal B cells, responses result from reduced expression of CD40L on T cells or reduced function of neonatal dendritic cells (Lewis 1998; von Hoegen et al. 1995) (Figure 14.3 and 14.9). Another theory proposes that the allergic response occurs when the amniotic fluid contains a high concentration of cytokines produced by decidual tissues (Jones et al. 2000). Maternal atopy has been shown to increase IgE levels in amniotic fluid (Jones et al. 1998) and, in fact, the allergens Der p1 of house dust mites and ovalbumin from hen's eggs have been detected in amniotic fluid (Bloomfield and Harding 1998). Fetuses swallow the amniotic fluid as well as aspirating it into their respiratory tract; furthermore, fetal skin is highly permeable and direct exposure may occur (Bloomfield and Harding 1998; Jones et al. 1998). Fetal gut has the most mature immune active tissues; several types of fully effective APC concentrate in rudimentary Peyer's patches early in the second trimester of pregnancy. The necessary costimulatory signals facilitate antigen presentation by these APC to T lymphocytes, and the APC have high- and low-affinity receptors for IgE as well as for IgG. Thus, the potential exists for sensitization to occur in utero (Warner and Jones 2000).
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