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Cited by 524

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A Critical Role for Murine Complement Regulator Crry in Fetomaternal Tolerance

Xu, Chenguang, Mao, Dailing, Holers, V. Michael, Palanca, Ben, Cheng, Alec M., Molina, Hector·2000·Science

Abstract

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.

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Metadata

Authors
Xu, C., Mao, D., Holers, V. M., Palanca, B., Cheng, A. M., & Molina, H.
Venue
Science
Published
2000-01-21
Volume
287
Issue
5452
Pages
498-501
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W1659820601
Cited by
524
References
0
FWCI
10.80
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: A Critical Role for Murine Complement Regulator Crry in Fetomaternal Tolerance. https://app.cochat.ai/papers/10.1126/science.287.5452.498
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Xu, C., Mao, D., Holers, V. M., Palanca, B., Cheng, A. M., & Molina, H. (2000). A Critical Role for Murine Complement Regulator Crry in Fetomaternal Tolerance. Science. https://doi.org/10.1126/science.287.5452.498

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.