A Critical Role for Murine Complement Regulator Crry in Fetomaternal Tolerance
Chenguang Xu,
1*
Dailing Mao,
1*
V. Michael Holers,
2
Ben Palanca,
1
Alec
M. Cheng,
1
Hector Molina
13
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.
1 Departments of Medicine and Pathology,
Washington University School of Medicine, St. Louis, MO 63110, USA.
2 Departments of Medicine and Immunology, University
of Colorado Health Science Center, Denver, CO 80262, USA.
3 Veteran's Administration Medical Center, St.
Louis, MO 63106, USA.
*
These authors contributed equally to this work.
To whom correspondence should be addressed. E-mail:
hmolina{at}imgate.wustl.edu
