Disease-associated autoantibodies during pregnancy and at birth in families affected by type 1 XXXX .

@entity1 @entity9217 @entity6 @entity367
We studied the pattern of type 1 @entity6 -associated autoantibodies during pregnancy and the transplacental transfer of these autoantibodies to the fetal circulation and searched for possible signs of prenatal induction of beta-cell autoimmunity in newborn @entity1 . The population comprised 208 mothers and their newborn @entity1 . Seventy-four of the mothers (36%) had type 1 @entity6 and 134 (64%) of the @entity1 had an affected father or sibling. Blood samples were obtained from the mother at the end of the first trimester and at delivery, and from the cord blood of the newborn @entity1 . Close to 40% of the mothers with type 1 @entity6 had antibodies to islet cells (ICA), 55% to @entity367 decarboxylase (GADA) and 54% to the @entity9217 protein (IA-2A) in early pregnancy, whereas the corresponding frequencies in the nonaffected mothers were 5.2%, 5.2% and 3.0%. No significant changes could be seen in autoantibody levels during pregnancy, and there was a close correlation between the two maternal samples. One third of the @entity1 of mothers with type 1 @entity6 tested positive for ICA, 50% for GADA and 51% for IA-2A. Six percent of the @entity1 of nondiabetic mothers had ICA, 2.2% GADA and none had IA-2A. None of the @entity1 of the antibody negative mothers had antibodies in their cord blood. These observations indicate that the immunomodulatory effect of pregnancy on signs of beta-cell autoimmunity is weak, but if @entity6 -associated autoantibodies are present in the mother, most of them are transferred to the fetal circulation. Our data do not provide any support for fetal induction of beta-cell autoimmunity.
