PARENTAL HLA COMPATIBILITY, FETAL WASTAGE AND NEURAL-TUBE DEFECTS - EVIDENCE FOR A T/T-LIKE LOCUS IN HUMANS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 36  (5) , 1082-1091
Abstract
To test the hypothesis that a locus in or near the human major histocompatibility complex (HLA) contributes to both involuntary fetal loss and neural tube defects (NTD), sharing of antigens of the HLA-A, HLA-B or HLA-DR loci was evaluated in couples who had 3 or more 1st-trimester spontaneous abortions or who had a child with an NTD (myelomeningocele or anencephaly). HLA-A antigen sharing was increased in couples with 3 or more spontaneous abortions and in couples who had an anencephalic fetus, when compared with couples who had 3 or more pregnancies and no fetal loss. Increased sharing of antigens at the HLA-A and B loci was not seen in the entire group of couples with children with myelomeningocele, but was found in the subgroup of 36 couples whose child had a lumbar myelomeningocele. An increase in HLA-DR sharing was not seen in any group or subgroup when compared with the control couples. Among the aborting couples, increased sharing was not restricted to the couples who had no term pregnancies, but was also found in the couples whose fetal losses occurred after 1 or more normal term pregnancies. These results are consistent with the hypothesis that a locus on the HLA-A side of the HLA-DR locus contributes to some fetal loss and susceptibility to NTD. This model is proposed as an alternative to the hypothesis that the maternal immune response to paternal major histocompatibility complex (MHC) antigens is the basis for the increased HLA sharing in couples with fetal wastage.