Abstract
The fetus inherits and expresses paternal antigens and is therefore semiallogeneic to the maternal immune system. Acceptance of the ‘foreign’ fetus is imperative for a successful pregnancy and depends on regulation, rather than suppression of the materno-fetal alloimmune response. Improper regulation of the materno-fetal alloimmune response can have adverse effects
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on pregnancy and on the health of the neonatal calf. Two disorders representing different aspects of improper regulation of materno-fetal alloimmunity were studied: Retained Fetal Membranes, associated with absence (or reduction) of materno-fetal alloimmunity and Bovine Neonatal Pancytopenia, caused by iatrogenic boosting of materno-fetal alloimmunity.
Retention of the fetal membranes longer than normal (over 12 to 24 hours) is called retained fetal membranes (RFM) and is a common reproductive disorder of cattle. Results show that MHC class I compatibility between dam and calf gave a high risk of RFM. We conclude that around parturition allogeneic major histocompatibility complex (MHC) class I expressed on fetal trophoblasts elicits a materno-fetal alloimmune response that aids in the “loss” of fetal-maternal adherence. Conversely, absence (or reduction) of materno-fetal alloimmunity in MHC class I compatible pregnancies may lead to RFM. The coefficient of relationship between dam and calf is correlated with the probability of MHC class I compatibility between dam and calf and there was an effect of the coefficient of relationship on the occurrence of retained placenta. Additional findings indicate that RFM following induction of parturition with corticosteroids is associated with failure of the immune assisted loss of fetal-maternal adherence.
Bovine Neonatal Pancytopenia (BNP), a bleeding syndrome of neonatal calves, is caused by alloantibodies absorbed from the colostrum of particular cows and is characterized by loss of thrombocytes, leukocytes and bone marrow cells. Pregsure© BVD is the likely source of alloantigens inducing BNP-associated alloantibodies in the dam. It was found that the development of BNP in calves is a heritable trait of the dam rather than the calf and that genetic differences between BNP and non-BNP dams are likely due to genes controlling the quantitative alloantibody response following vaccination. We show that although the BNP-associated vaccine-induced maternal alloantibodies have heterogeneous specificities, pathogenicity appears to be mediated by MHC class I specific BNP alloantibodies alone. Furthermore, results indicate that the pathogenic effects of BNP alloantibodies correlate with alloantibody binding and that cells with high MHC class I expression were preferentially affected in BNP.
The fetus is semiallogeneic to the maternal immune system and regulation of the materno-fetal alloimmune response is essential for successful pregnancy and to avoid the transfer of pathogenic maternal alloantibodies.
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