Publication Date:
2000-01-22
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, C -- Mao, D -- Holers, V M -- Palanca, B -- Cheng, A M -- Molina, H -- R01 AI40576-01/AI/NIAID NIH HHS/ -- R01 AI44912-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):498-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642554" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
*Complement Activation
;
Complement C3/analysis/immunology
;
Embryo, Mammalian/*immunology/metabolism
;
*Embryonic and Fetal Development
;
Female
;
Gene Targeting
;
*Immune Tolerance
;
Mice
;
Neutrophil Infiltration
;
Pregnancy
;
Receptors, Complement/genetics/*physiology
;
Trophoblasts/immunology/metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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