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The reason for their emergence remains unknown. Taken the above numbers, the infusion of human-derived products containing IgA resulting in severe anaphylactoid type AEs should be considerable. This is not the case (39). Questions about the clinical relevance of above numbers emerge as soon as blood banks (i) estimate the theoretical risk of IgA anaphylactic reactions (32); (ii) assess the relation of severe IgAD with the presence or absence of anti-IgA antibodies (40); (iii) screen donors for very low IgA levels in order to become able to provide blood and plasma-derived products free of IgA and find a UGT1A7 considerably lower frequency than expected (41). Alternatively, the test systems may not reliably detect anti-IgA antibodies being as yet insensitive and inaccurate or �C at least �C do not correspond to the clinically relevant learn more fraction of antibodies. This comes to mind when a more close look to ��anti-IgA�� gives ��unexpected�� results, including ��anti-IgA�� in blood donors with normal serum IgA level or ��anti-IgA�� that cannot be neutralized with purified IgA (42); or when blood products containing proven anti-IgA do not elicit severe AEs (43). Among patients on replacement therapy, those with CVID may rarely develop severe immediate AEs (32). The discrepancy between anti-IgA positive patients and frequency of AEs raises the question about the nature of the many reported anti-IgA antibodies and also raises the question about the immunologic condition which allows the formation of anaphylactoid anti-IgA antibodies. There might be some logic in supposing that anaphylactoid anti-IgA cannot evolve at IgA levels otherwise fulfilling the definition of IgAD. Such a condition would constantly generate ICs which in turn could activate complement, react with immune cells, and be deposited in lung and kidney. Indeed, Horn et al. found anti-IgA antibodies R428 solubility dmso in CVID patients missing IgA+ B cells and presenting with IgA levels