Immune aspects of pathology of the placental bed contributing to pregnancy pathology.
Interest has recently focused on the role of the placental bed in the pathogenesis of a variety of pregnancy disorders. Considerable advances have been made in the understanding of the complex relationships between maternal and fetal trophoblast in the placental bed in normal pregnancy. Invasion of uterine spiral arteries by extravillous trophoblast effects the physiological changes required to accommodate increased blood flow to the fetoplacental unit. Control of trophoblast invasion may depend on intrinsic properties, such as production of proteolytic enzymes and expression of a non-classical class I MHC antigen, but maternal cells within decidua may also play a role. Leukocytes form a major component of human decidualized endometrium and in the first trimester consist of granulated lymphocytes, macrophages and T lymphocytes. Suggested roles for decidualized leukocytes include natural killer cell activity, cytokine secretion, antigen presentation and immunosuppression. Several pregnancy disorders, including pre-eclampsia and intrauterine growth retardation, may be due to abnormal maternofetal cellular relationships within the placental bed causing inadequate invasion of spiral arteries and acute atherosis. However, the role of immunological factors in the pathogenesis of these disorders is uncertain since deposition of immunoglobulins and complement has also been detected in spiral arteries in normal pregnancy. Placenta accreta may reflect undue invasiveness of trophoblast and immunohistochemical studies of subinvolution of uteroplacental arteries also suggest an abnormal maternofetal relationship in the placental bed. Although the in vivo role of decidual leukocytes is not known, studies of infertile endometrium have reported a deficiency of granulated lymphocytes, suggesting a possible role in early implantation and placentation. Granulated lymphocytes may also play a role in pregnancy loss. There have been considerable advances in understanding of the abnormal maternofetal relationships in the placental bed which can lead to pregnancy disorders. However, the aetiology and pathogenesis of the various clinical conditions is unlikely to be fully established until regulatory mechanisms in normal pregnancy are elucidated.
Bulmer
J N
JN
School of Pathological Sciences, University of Newcastle upon Tyne, Royal Victoria Infirmary, UK.
D000022:Abortion, Spontaneous / Q000276:immunology; D003656:Decidua / Q000276:immunology; D005260:Female; D005317:Fetal Growth Retardation / Q000276:immunology; D006098:Granulocytes / Q000276:immunology; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D010920:Placenta / Q000276:immunology* / Q000473:pathology; D010921:Placenta Accreta / Q000276:immunology; D011225:Pre-Eclampsia / Q000276:immunology; D011247:Pregnancy / Q000276:immunology*; D011248:Pregnancy Complications / Q000209:etiology / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D014328:Trophoblastic Neoplasms / Q000276:immunology; D014327:Trophoblasts / Q000276:immunology