5.4.2. Asthma

Asthma is a chronic inflammatory disease of the respiratory system characterized by bronchial hyperresponsiveness and reversible airflow obstruction. It is one of the most common chronic illnesses in childhood and its etiology in this group is vastly associated with atopy. Some studies report that asthmatic patients are more likely to have a diagnosis of sIgAD/CVID than non-asthmatic individuals [134]. In a study on an Iranian group, the prevalence of asthma among sIgAD patients was 51% [10], while in the general Iranian population it is 22–23% [135,136]. In the study on a Spanish group, asthma was observed in only 12.4% patients [97]. On the other hand, no difference in prevalence was found comparing sIgAD patients and control group in the case-control study of Jorgensen et al. [137]. The prevalence of asthma among patients with SIgAD is presented in Table 2.

Papadopoulou et al. state that the insufficient protection provided by the respiratory mucosa deprived of IgA in children with sIgAD makes them prone to develop bronchial hyperresponsiveness and consequently asthma [138]. In a different study, a high number of IgA-specific salivatory antibodies has been connected to a lower risk of late-onset wheezing in sensitized infants [139]. Furthermore, sIgAD may be connected with TNFRSF13B gene variants as one of the genetic susceptibilities. This gene encodes the transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), which is the tumor necrosis factor receptor (TNFR) expressed on activated B cells and macrophages and is involved in isotype class switching to IgA [54,140,141]. Moschese et al. investigated the prevalence of TNFRSF13B mutations in 56 patients with absolute and partial sIgAD reporting 20% prevalence in this group [142]. Furthermore, researchers suggest that the mutation in these genes increases the risk of asthma development up to 2.5 fold, despite the IgE levels [69]. Moreover, the studies on the mice model proved that treating with antigen-specific IgA may protect animals from hyperresponsiveness as well as eosinophilic inflammation in airways [143]. Additionally, since mice do not express FcαRI [144], studies on human FcαRI transgenic mice were used in studies on the asthma model. It was found that by targeting FcαRI, IgA has been established as a strong inhibitor of asthma development [145].

Some studies reported a higher prevalence of respiratory tract infections among patients with sIgAD and allergy compared to those with sIgAD without any manifestation of allergy disease [99,133,146]. It suggests that allergic patients are more susceptible to respiratory tract infections.


**Table 2.** Asthma and sIgAD.
