Autoantibodies in normal and abnormal pregnancy.
Abnormal autoimmune function has been associated with reproductive failure for decades. In fact, all medical conditions historically associated with pregnancy loss (and on occasion infertility) are now recognized to have an autoimmune etiology. It is therefore quite surprising that only less than a decade ago a correlation between the presence of abnormal autoantibodies and pregnancy loss was reported for the first time. Since reproductive failure, similar to other abnormal autoimmune states, is not a monoclonal event, we have established that affected patients demonstrate polyclonal autoantibody abnormalities including a variety of nonorganospecific as well as organspecific autoantibody groupings. For example, patients with repeated pregnancy loss will exhibit abnormal levels of anti-phospholipid antibodies (PA). In normal pregnancy natural autoantibodies do not follow the standard immunoglobulin (Ig) pattern, characterized by a decrease in levels despite a probably mild increase in production, which is excessively compensated by the vasodilatation of pregnancy. PA, especially, demonstrate a mild increase during pregnancy, though levels only in the peripartal period may reach abnormally high titers (in comparison to nonpregnant controls). This dichotomy between total Ig and natural autoantibodies is interesting since it suggests that autoantibodies may be under distinct control. In fact, we have suggested that this observed elevation of autoantibodies may be the result of an antigenic stimulus by self-like antigen, represented by the maternal growth of the parasitic fetus. In abnormal pregnancies, especially those associated with maternal hypertension and fetal growth retardation (IUGR), autoantibody levels do reach highly abnormal levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Gleicher
N
N
Center for Human Reproduction, Chicago, IL 60610.
D000026:Abortion, Habitual / Q000209:etiology / Q000276:immunology; D017152:Antibodies, Antiphospholipid / Q000032:analysis; D016736:Antiphospholipid Syndrome / Q000276:immunology / Q000503:physiopathology; D001323:Autoantibodies / Q000032:analysis*; D001324:Autoantigens / Q000276:immunology / Q000378:metabolism; D001327:Autoimmune Diseases / Q000150:complications / Q000276:immunology*; D015551:Autoimmunity; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000276:immunology; D005333:Fetus / Q000276:immunology*; D006801:Humans; D008431:Maternal-Fetal Exchange; D011225:Pre-Eclampsia / Q000276:immunology; D011247:Pregnancy / Q000276:immunology*; D011248:Pregnancy Complications / Q000276:immunology*
D017152:Antibodies, Antiphospholipid; D001323:Autoantibodies; D001324:Autoantigens