A critical role for murine complement regulator Crry in fetomaternal tolerance

被引：399

作者：

Xu, CG

Mao, DL

Holers, VM

Palanca, B

Cheng, AM

Molina, H ^{[1
]}

机构：

[1] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA

[3] Univ Colorado, Hlth Sci Ctr, Dept Med, Denver, CO 80262 USA

[4] Univ Colorado, Hlth Sci Ctr, Dept Immunol, Denver, CO 80262 USA

[5] Vet Adm Med Ctr, St Louis, MO 63106 USA

来源：

SCIENCE | 2000年 / 287卷 / 5452期

关键词：

D O I：

10.1126/science.287.5452.498

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：498 / 501

页数：4

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