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 c omplement regulator decay accelerating factor were normal. Mice that were d eficient in another murine complement regulator, Crry, were generated to in vestigate its role in vivo. Survival of Crry(-/-) embryos was compromised b ecause of complement deposition and concomitant placenta inflammation. Comp lement activation at the fetomaternal interface caused the fetal Loss becau se breeding to C3(-/-) mice rescued Crry(-/-) mice from lethality. Thus, th e regulation of complement is critical in fetal control of maternal process es that mediate tissue damage.