Individual variations

Post-natal mucosal B-cell development shows large individual variations, even within the same population (Brandtzaeg et al., 1991). This disparity could partly reflect a genetically determined effect on the establishment of the mucosal barrier function. Thus, it has been proposed, on the basis of serum IgA levels, that a hereditary risk of atopy is related to a retarded post-natal development of the IgA system (Taylor et al., 1973; Soothill, 1976). This notion was later supported by a report showing significantly reduced IgA immunocyte numbers (with no compensatory IgM enhancement) in the jejunal mucosa of atopic children (Sloper et al., 1981). Also, an inverse relationship was found between the serum IgE level and the jejunal IgA cell population in children with food-induced atopic eczema (Perkkio, 1980). It was subsequently reported that infants born to atopic parents showed a significantly higher prevalence of salivary IgA deficiency than age-matched control infants (van Asperen et al., 1985). Interestingly, Kilian et al. (1995) found that the throats of 18-month-old infants with presumably IgE-mediated allergic problems contained significantly higher proportions of IgA1 protease-producing bacteria than age-matched healthy controls, thus supporting a previous report showing much less intact IgA in nasopharyngeal secretions from children with a history of atopic allergy than from controls with episodes of acute otitis (S0rensen and Kilian, 1984). In this context, it is important to note that it takes up to 3 months after birth before the IgA2-to-IgA1 immunocyte ratio in salivary glands has increased to the adult value, with approximately 33% IgA2-producing cells (Thrane et al., 1991). 2

Altogether, a poorly developed or enzymatically reduced SIgA-dependent mucosal barrier function, combined with a hereditary and/or cytokine-driven hyper-IgE responsiveness (see below), could contribute to the pathogenesis of allergy. This notion accords with the increased frequency not only of infections, but also of atopic allergy and coeliac disease seen in subjects with permanent selective IgA deficiency (Burrows and Cooper, 1997), although compensatory over-production of SIgM may apparently counteract the adverse consequences of their absent mucosal IgA responses, particularly in the gut (Brandtzaeg et al., 1991; Brandtzaeg and Nilssen, 1995).

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