Porcine IgA allotypes are not equally transcribed or expressed in heterozygous swine
Is Version Of
The prediction of 1:1 expression of constant region allotypes in heterozygous animals assumes that productive VDJ rearrangements occur at random between chromosomes, switch recombination is random, there is no allele-related defect in switching and there is no selection for a B-cell receptor bearing a certain constant region allotype. In data reported here, this prediction was often not fulfilled for the transcripts encoding the IgAa and IgAb alleles of porcine IgA including those from late term fetal piglets that are not in contact with environmental antigens or maternal regulatory factors. In the spleen, thymus, mesenteric lymph node (MLN), ileal Peyer patches, parotid gland and PBLs of 5-week-old conventionally-reared Duroc pigs, ratios of IgAa to IgAb transcripts as high as 4:1 were observed. Since White Cross animals had significantly higher levels of IgAb than IgAa (some >3-fold), a allele-linked switch defect cannot explain the deviation from the expected 1:1 ratio. When the IgAa:IgAb ratios in older Durocs and those reared at a different site were studied, no evidence for breed dependence of differential transcription was found. Total serum IgA levels paralleled total transcript levels in PBLs while particularly in White Cross animals, the IgAa:IgAb ratio in serum was higher in many animals than the IgAa:IgAb transcript ratio in their PBLs. We conclude that deviations from the expected 1:1 ratio of allotype transcripts and secreted IgA in young pigs is normal and deviations from this ratio also occur during fetal life in the absence of environmental antigens and maternal regulatory factors. We speculate that postnatal deviations result from: (a) exposure to environmental antigens that selectively expand B-cells expressing VH gene alleles linked to either IgAa or IgAb or (b) some form of colostrum-dependent regulation. Pre-natal regulation may depend on the selection of B-cells bearing certain VH or CH encoded BCRs by stromal ligands such as fetal B-cell superantigens.
This is an article from Molecular Immunology 37 (2000): 653, doi:10.1016/S0161-5890(00)00086-9. Posted with permission.