Lack of classical HLA antigens on trophoblast has been postulated as an argument against the hypothesis that foetal rejection is akin to allograft rejection. However, downregulation of HLA-G molecules and increased expression of classical HLA antigens were documented in recurrent pregnancy loss and pre-eclampsia pregnancies. The sparce presence of anti-HLA antibodies in recurrent pregnancies loss patients resulted probably from the failure to carry gestation long enough to produce response. They could originate from recognition of classical HLA antigens expressed on small remnants of trophoblast and foetal membranes exposed to maternal effector cells "cleaning up" uterine cavity post-delivery. Anti-HLA antibodies are not able to affect adversely the next pregnancy with the same partner, as classical HLA targets are hidden, and trophoblast exposed to maternal immune recognition is protected by HLA-G.
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