A critical role for murine complement regulator Crry in fetomaternal tolerance

Chenguang Xu, Dailing Mao, V. Michael Holers, Ben Palanca, Alec M. Cheng, Hector Molina

Research output: Contribution to journalArticlepeer-review

440 Scopus citations


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.

Original languageEnglish
Pages (from-to)498-501
Number of pages4
Issue number5452
StatePublished - Jan 21 2000


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