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ANTI‐IgA ANTIBODIES OF LIMITED SPECIFICITY IN HEALTHY IgA DEFICIENT SUBJECTS
Author(s) -
Koistinen J.,
Cardenas R. M.,
Fudenberg H. H.
Publication year - 1977
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.1977.tb00912.x
Subject(s) - allotype , subclass , antibody , iga deficiency , hemagglutination , immunoglobulin a , immunology , antigen , biology , immunoglobulin g
SUMMARY To investigate the subclass and allotype specificity of anti‐IgA antibody synthesis, serum samples from 156 IgA deficient blood donors were screened for anti‐IgA antibodies by passive haemagglutination using IgA proteins of both subclasses (IgA1 and IgA2) as well as allotypes A 2 m(1) and A 2 m(2). Anti‐IgA activity was found in 25% (thirty‐nine). Antibodies were class‐specific in 19% (twenty‐nine) and of limited specificity in 6% (ten) of the samples. One unusual serum had anti‐IgA directed solely against IgA2. Its activity against A 2 m(2) was inhibited not only by A 2 m(2) protein but also by A 2 m(1) and by three IgA1 proteins. The anti‐A 2 m(1) activity of the same sample was inhibited only by A 2 m(1) proteins. The specific mechanism of IgA deficiency in this sample is discussed as well as the structural differences of the different allo‐ and subtypes of IgA and their relation to the antigenic properties of IgA. Inhibition studies could be performed with only one sample with anti‐IgA1 antibodies, but no allotypes of IgA1 were found. By haemagglutination inhibition, 15% (twenty‐three) of the samples contained minute amounts of IgA1, but no IgA2. None of the samples had only IgA2 or IgA1 and IgA2. Both findings, anti‐IgA antibodies with limited specificity in IgA deficient subjects and minute amounts of IgA of one subclass only in IgA deficient samples, are conceivable if IgA deficiency is caused by selective lack or defect of a subclass of B lymphocytes specifically synthesizing IgA2.