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

Authors

P. Navarro, University of Iowa
R.K. Christensen, USDA, ARC
P. Weber, University of Iowa
M. Rothschild, University of Iowa
G. Ekhardt, Pig Improvement Corporation
J.E. Butler, University of IowaFollow

Date of this Version

2000

Document Type

Article

Citation

Molecular Immunology 37 (2000) 653–664; PII: S0161-5890(00)00086-9

Abstract

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 IgA^a and IgA^b 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 IgA^a to IgA^b transcripts as high as 4:1 were observed. Since White Cross animals had significantly higher levels of IgA^b than IgA^a (some >3-fold), a allele-linked switch defect cannot explain the deviation from 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 dependence of differential transcription was found. Total serum IgA levels paralleled total transcript levels in PBLs while particularly in White Cross animals, 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 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 V_H gene alleles 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 bearing certain V_H or C_H encoded BCRs by stromal ligands such as fetal B-cell superantigens.