Abstract
Total levels of IgM and secretory IgM as well as specific antibodies to poliovirus type I antigen,Escherichia coli O antigens, and β-lactoglobulin were measured in unstimulated and stimulated saliva as well as nasal secretion using an enzyme-linked immunosorbent assay (ELISA). The levels of these antibodies in IgA-deficient adults with and without frequent respiratory infections and children under immunosuppressive therapy for malignant disease were compared to those in normal adults and infants 1–7 months of age. The IgA-deficient adults had significantly higher IgM levels (P<0.002) than the normal adults as well as higher levels of IgM antibodies to poliovirus type I (P<0.05) andE. coli O antigen (P<0.002). There was a less pronounced IgM anti-β-lactoglobulin compensation. Secretory component (SC)-carrying antibodies against all three antigens were lower than in normal adults. The infants studied had levels of IgM in secretions close to those of the normal adults and significantly lower than those of the IgA-deficient adults (P<0.001) but with a higher proportion of SC-carrying IgM. The increase in total IgM and specific bacterial and viral IgM antibodies in saliva above that of the normal adults was significant(P<0.001–0.005) for those IgA-deficient individuals without, but not for those with, frequent infections. There was, however, no significant difference between the levels in the two groups of IgA-deficient adults. The total levels of SIgA and specific antibodies toE. coli O antigens and poliovirus type I antigen in saliva from children treated with multiple cytotoxic drugs for malignant disease did not differ from normal levels, irrespective of the duration of treatment. The lower IgM levels in saliva of IgA-deficient individuals with many infections was seen in spite of their frequent infections, suggesting a primary defect in an important compensatory defense mechanism.
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Mellander, L., Björkander, J., Carlsson, B. et al. Secretory antibodies in IgA-deficient and immunosuppressed individuals. J Clin Immunol 6, 284–291 (1986). https://doi.org/10.1007/BF00917328
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DOI: https://doi.org/10.1007/BF00917328