title: Immunological modes of pregnancy loss.
abstract: During the implantation period, a significant portion of embryos are lost and eventually less than half of clinically established pregnancies end as full-term pregnancies without obstetrical complications. A significant portion of these pregnancy losses is associated with immune etiologies, including autoimmune and cellular immune abnormalities. Although an autoimmune etiology such as anti-phospholipid antibodies (APAs) has been reported to induce placental infarct and thrombosis at maternal-fetal interface, APAs induce inflammatory immune responses as well. Inflammatory immune responses, such as increased proportions of NK cells and Th1/Th2 cell ratios in peripheral blood are related to recurrent pregnancy losses and multiple implantation failures. Systemic and local inflammatory immune responses seem to be induced by activation of Toll-like receptors with infectious agents, fetal cell debris, or gonadotropin-releasing hormone agonist, etc. Cellular activation of T and NK cells leads to pro-inflammatory cytokine storm and consequently, placental infarction and thrombosis. Potential application of anti-inflammatory therapeutic agents for the prevention of pregnancy losses should be explored further.
authors.affiliation: Reproductive Medicine Program, Department of Obstetrics and Gynecology, The Chicago Medical School at Rosalind Franklin University of Medicine and Science, Vernon Hills, IL, USA. joanne.kwakkim@rosalindfranklin.edu
authors.forename: Joanne
authors.initials: J
authors.lastname: Kwak-Kim
authors.forename: Joon Cheol
authors.initials: JC
authors.lastname: Park
authors.forename: Hyun Kyong
authors.initials: HK
authors.lastname: Ahn
authors.forename: Joon Woo
authors.initials: JW
authors.lastname: Kim
authors.forename: Alice
authors.initials: A
authors.lastname: Gilman-Sachs
mesh_terms: D000818:Animals; D001778:Blood Coagulation Disorders / Q000150:complications / Q000276:immunology; D010064:Embryo Implantation / Q000276:immunology; D020964:Embryo Loss / Q000209:etiology* / Q000276:immunology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D011247:Pregnancy; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology