Porcine IgA allotypes are not equally transcribed or expressed in heterozygous swine

The prediction of 1:1 expression of constant region allotypes in heterozygo us animals assumes that productive VDJ rearrangements occur at random betwe en 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 IgA(a) and IgA(b) alleles of porcine IgA including those from late term fetal piglets that a re not in contact with environmental antigens or maternal regulatory factor s. In the spleen, thymus, mesenteric lymph node (MLN), ileal Peyer patches, parotid gland and PBLs of 5-week-old conventionally-reared Duroc pigs, rat ios of IgA(a) to IgA(b) transcripts as high as 4:1 were observed. Since Whi te Cross animals had significantly higher levels of IgA(b) than IgA(a) (som e > 3-fold), a allele-linked switch defect cannot explain the deviation fro m the expected 1:1 ratio. When the IgA(a):IgA(b) ratios in older Durocs and those reared at a different site were studied, no evidence for breed depen dence of differential transcription was found. Total serum IgA levels paral leled total transcript levels in PBLs while particularly in White Cross ani mals, the IgA(a):IgA(b) ratio in serum was higher in many animals than the IgA(a):IgA(b) transcript ratio in their PBLs. We conclude that deviations f rom the expected 1:1 ratio of allotype transcripts and secreted IgA in youn g pigs is normal and deviations from this ratio also occur during fetal lif e in the absence of environmental antigens and maternal regulatory factors. We speculate that postnatal deviations result from: (a) exposure to enviro nmental antigens that selectively expand B-cells expressing V-H gene allele s linked to either IgA(a) or IgA(b) or (b) some form of colostrum-dependent regulation. Pre-natal regulation may depend on the selection of B-cells be aring certain V-H or C-H encoded BCRs by stromal ligands such as fetal B-ce ll superantigens. (C) 2001 Elsevier Science Ltd. All rights reserved.