Negligible role of antibodies and C5 in pregnancy loss associated exclusively with C3-dependent mechanisms through complement alternative pathway.
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.
Mao
Dailing
D
Rheumatology Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Wu
Xiaobo
X
Deppong
Christine
C
Friend
Lindzy D
LD
Dolecki
Gregory
G
Nelson
D Michael
DM
Molina
Hector
H
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
D003176:Complement C3; D003182:Complement C5