A Critical Role for Murine Complement Regulator Crry in Fetomaternal Tolerance

Complement is a component of natural immunity. Its regulation is needed to protect tissues from inflammation, but mice with a disrupted gene for the complement regulator decay accelerating factor were normal. Mice that were deficient in another murine complement regulator, Crry, were generated to in...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2000-01, Vol.287 (5452), p.498-501
Main Authors: Xu, Chenguang, Mao, Dailing, Holers, V. Michael, Palanca, Ben, Cheng, Alec M., Molina, Hector
Format: Article
Language:English
Subjects:
Animals
Antibodies
Biological and medical sciences
Complement Activation
Complement C3 - analysis
Complement C3 - immunology
Crry protein
Developmental Stages
Embryo, Mammalian - immunology
Embryo, Mammalian - metabolism
Embryonic and Fetal Development
Embryos
Female
Fundamental and applied biological sciences. Psychology
Gene expression regulation
Gene Targeting
Histones
Immune Tolerance
Inflammation
Magnification
Medical research
Mice
Mother. Fetoplacental unit. Mammary gland. Milk
Neonates
Neutrophil Infiltration
Pregnancy
Pregnancy. Parturition. Lactation
Receptors, Complement - genetics
Receptors, Complement - physiology
Regulator genes
Rodents
Trophoblasts - immunology
Trophoblasts - metabolism
Ubiquitins
Vertebrates: reproduction
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Summary:Complement is a component of natural immunity. Its regulation is needed to protect tissues from inflammation, but mice with a disrupted gene for the complement regulator decay accelerating factor were normal. Mice that were deficient in another murine complement regulator, Crry, were generated to investigate its role in vivo. Survival of Crry-/-embryos was compromised because of complement deposition and concomitant placenta inflammation. Complement activation at the fetomaternal interface caused the fetal loss because breeding to C3-/-mice rescued Crry-/-mice from lethality. Thus, the regulation of complement is critical in fetal control of maternal processes that mediate tissue damage.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.287.5452.498