Document Detail


Negligible role of antibodies and C5 in pregnancy loss associated exclusively with C3-dependent mechanisms through complement alternative pathway.
MedLine Citation:
PMID:  14670299     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Dailing Mao; Xiaobo Wu; Christine Deppong; Lindzy D Friend; Gregory Dolecki; D Michael Nelson; Hector Molina
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Immunity     Volume:  19     ISSN:  1074-7613     ISO Abbreviation:  Immunity     Publication Date:  2003 Dec 
Date Detail:
Created Date:  2003-12-12     Completed Date:  2004-01-21     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9432918     Medline TA:  Immunity     Country:  United States    
Other Details:
Languages:  eng     Pagination:  813-22     Citation Subset:  IM    
Affiliation:
Rheumatology Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
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MeSH Terms
Descriptor/Qualifier:
Abortion, Spontaneous / immunology,  metabolism*
Animals
Complement C3 / metabolism*
Complement C5 / metabolism
Complement Pathway, Alternative / physiology*
Female
Mice
Placenta / metabolism,  pathology
Pregnancy
Grant Support
ID/Acronym/Agency:
R01 AI40576/AI/NIAID NIH HHS; R01 AI44912/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Complement C3; 0/Complement C5

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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