5.4.1. Food Allergy

The prevalence of food allergy in patients with PIDs was examined using the US Immunodeficiency Network (USIDNET). Surprisingly, it was lower than that in the general population. However, for some specific types of PID, like sIgAD, the prevalence was increased and it was found to be 25% [123], but there were only four patients with sIgAD in the registry. It is consistent with the study performed by Aghamohammadi et al. where the prevalence of food allergy among patients with sIgAD was 22% [10]. Across all studies in this review, the prevalence of food allergy among patients with SIgAD is presented in Table 1. Another study reports an increased risk of parentally reported food hypersensitivity at 4 years of age among children with sIgAD [124]. Moreover, the authors did not find any association between IgAD and increased levels of specific IgE, which could suggest that hypersensitivity in IgAD children is not IgE-mediated [124].

The majority of patients with deficiency of secretory IgA have substitution with secretory IgM. However, it might not guarantee proper mucosal protection and might allow food antigens to pass through the gastrointestinal mucosa and predispose to develop a food allergy. Another possible explanation connected with eczema and food allergy is the hypothesis that, due to the IgA-deficiency to gastrointestinal antigens in the gut, there is no antigen immunological-exclusion, which consists of antigen binding to SIgA at the level of the mucosal surface, and, consequently, blocking the absorption of the antigen [9,125].

Recent years showed that there is a strong connection between microbiota and allergy development. For example, in 2009, researchers found that children with allergy not only had lower salivary SIgA levels but also less differentiated bacterial microenvironment [126,127]. A study from 2018 focused on the effects of IgA deficiency on human gut microbiota composition [128]. They found out that patients with sIgAd have an altered gut microbiota composition compared to healthy patients. Moreover, the secretion of IgM cannot fully compensate for the lack of SIgA. It is therefore suggested that IgA plays a

critical role in controlling stable gut microbial community. A different study from the same year showed only mild loss in microbial diversity in sIgAD subjects [129].

It was also found that serum IgA plays a role in suppressing IgE-mediated food allergy. IgE-mediated food allergy is a common cause of enteric disease, and, in the study conducted by Strait et al. concerning IgE-mediated systemic anaphylaxis induced by ingested allergens, it has been found that both serum antigen-specific IgG and IgA antibodies can protect against severe IgE-mediated allergic reaction [130]. This suggests that decreased serum IgA antibody levels might predispose to increased intestinal mucosal permeability and absorption of ingested antigens, therefore, increasing the risk of severe food allergy [131].


