This relationship is evident in some immunity disorders such as CVID [191,192]. (e.g., eczema, rhinitis, asthma) are more common in patients diagnosed with this particular PID. Selective IgA deficiency, although usually mildly symptomatic, can be difficult for clinicians. The aim of the study is to summarize the connection between selective IgA deficiency and atopic diseases. and annual vaccination against influenza [34]. It is not typically recommended to initiate IgG (i.v, s.c) replacement therapy in patients without the coexistence of other immune-related diseases, acute, severe infections, or coexistence of specific antibodies deficiency [81]. According to one of the latest meta-analyses covering the effects of oral probiotics, parabiotics, and synbiotics on immunoglobulin levels, it has been shown that their supplementation increases significantly salivary IgA secretion, without a significant effect on the level of other immunoglobulins and with no effect on the serum IgA [82]. In addition, there are reports of an increase in the amount of IgA+ cells in the intestines of lamina propria in mice after oral ingestion of Lactobacillus-based preparations [83,84]. One prospective, randomized study demonstrated the validity of the use of oral immunomodulator bacterial extract (OM-85 BV) in patients with sIgAD and/or IgG subclass deficiency, resulting in a lower one-year infection rate [85]. A suggestion has been made to use oral IgA in patients with sIgAD, since this deficiency is associated with dysbiosis and chronic inflammation, and the present inflammation is inversely correlated with systemic anticommensal IgG response, which acts as second line of defense SEL120-34A HCl [86,87]. The importance of the IgA was raised again because of the ongoing global pandemic of coronavirus disease 2019 (COVID-19). When looking for the reasons for the varied course of the disease, questions arose on whether deficiency of IgA could be the reason for disease severity, vaccine failure, and prolonged viral shedding [88]. As mentioned above, the prevalence of sIgAD differs in various countries and the same was found for COVID-19. Naito et al. compared the number of cases of COVID-19 with the prevalence of selective IgA deficiency in different countries [89]. They found a strong positive correlation between the frequency of sIgAD Rabbit Polyclonal to PE2R4 and the COVID-19 infection rate per population. It was then concluded that one of the factors contributing to the low death rate from COVID-19 infection in Japan could be the low incidence of sIgAD in the country. As primary immunodeficiencies are a group of rare diseases, there is little data on the coexistence of sIgAD and COVID-19 infection. Nevertheless, literature data showing an extremely significant effect of class A immunoglobulins on early protection against SARS-CoV-2 virus also suggest a potentially more severe/complicated course of the disease [88,90]. This thesis is supported by the aforementioned literature data: a positive correlation between a high number of COVID-19 infections and a high incidence of sIgAD has been demonstrated, and an inverse relationship was observed in the extreme SEL120-34A HCl example of Japan [88]. In Israel, during two so-called waves, 20 patients with PID were affected by COVID-19 and none of them was diagnosed with sIgAD [91]; importantly, the relationship between the development of autoimmune diseases in the course of COVID-19 in patients with sIgADAIHA and Guillain-Baree syndrome [92]. Researchers also point to the risk of a poor response against SARS-CoV-2 after immunization in this group of patients [88]. 5.3. Autoimmunity There is an association between IgA deficiency and a higher prevalence SEL120-34A HCl of autoimmune disease [93,94]. Based on extended research in that field, the prevalence of autoimmune disease in this group rises to 31.7% [95]. According to Azizi et al. the median age of the onset of the first episode of autoimmunity was 7 [95]. Among diseases with higher prevalence in sIgAD subjects, we differentiate systemic lupus erythematosus, hypo- and hyperthyroidism, type 1 diabetes mellitus, Crohns disease, ulcerative colitis, rheumatoid arthritis, juvenile idiopathic arthritis, ankylosing spondylitis, and vitiligo. Whereas other diseases like scleroderma, celiac disease, autoimmune hepatitis, immune thrombocytopenic purpura, and autoimmune hemolytic anemia, occur less often but still with higher prevalence than in the general population [96]. The SEL120-34A HCl mechanism of autoimmunity in sIgAD is still not fully understood. There are six hypotheses that try to explain these phenomena, each based on a different mode of autoimmunity, such as human leukocyte antigen, cytogenic, monogenic, molecular mimicry, lingering inflammation and immune complexes, dysregulation of molecular pathways [96]. Some.