Immunology of term and preterm labor.
During pregnancy there is an alteration in maternal immunity within the uterus where innate, proinflammatory immune responses are tightly regulated to prevent immunological rejection of the fetal allograft. Disruption of the delicate balance of cytokines by bacteria or other factors increases the production of proinflammatory cytokines at the maternal-fetal interface and activates the parturition mechanism prematurely. Despite years of searching, there is still no broadly effective strategy for preventing preterm labor and most therapies are directed at inhibiting myometrial contractions and improving neonatal outcome. Recent studies with progestins and interleukin-10 (IL-10), however, are showing promise in randomized clinical trials and animal studies. Furthermore, the identification of the Toll-like receptors as upstream mediators of inflammation may offer alternative therapeutic targets for preventing this common pregnancy complication.
Peltier
Morgan R
MR
Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, UT 84132, USA. mpeltier@hci.utah.edu
D005260:Female; D006790:Host-Parasite Interactions / Q000276:immunology; D006801:Humans; D007167:Immunotherapy; D007249:Inflammation / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000628:therapy; D007752:Obstetric Labor, Premature / Q000453:epidemiology / Q000209:etiology / Q000276:immunology* / Q000382:microbiology; D011247:Pregnancy; D047929:Term Birth / Q000276:immunology*