title: Negligible role of antibodies and C5 in pregnancy loss associated exclusively with C3-dependent mechanisms through complement alternative pathway.
abstract: Factors involved in pregnancy failure due to abnormal fetomaternal tolerance are poorly understood. Here we describe distinct defects in placenta formation and subsequent pregnancy loss solely dependent on the activation of the complement alternative pathway and the effector mechanisms provided by the maternal C3. Surprisingly, this effect is independent of other complement activation pathways and of the effector mechanisms provided by other complement components. These findings provide significant insight into the role of the innate immune system in human pregnancy failure, a frequent clinical outcome.
authors.affiliation: Rheumatology Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
authors.forename: Dailing
authors.initials: D
authors.lastname: Mao
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Wu
authors.forename: Christine
authors.initials: C
authors.lastname: Deppong
authors.forename: Lindzy D
authors.initials: LD
authors.lastname: Friend
authors.forename: Gregory
authors.initials: G
authors.lastname: Dolecki
authors.forename: D Michael
authors.initials: DM
authors.lastname: Nelson
authors.forename: Hector
authors.initials: H
authors.lastname: Molina
mesh_terms: D000022:Abortion, Spontaneous / Q000276:immunology / Q000378:metabolism*; D000818:Animals; D003176:Complement C3 / Q000378:metabolism*; D003182:Complement C5 / Q000378:metabolism; D003170:Complement Pathway, Alternative / Q000502:physiology*; D005260:Female; D051379:Mice; D010920:Placenta / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy
chemical_list: D003176:Complement C3; D003182:Complement C5