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Crry deficiency in complement sufficient mice: C3 consumption occurs without associated renal injury

Ruseva, Marieta Milkova, Hughes, Timothy Richard ORCID:, Donev, Rossen Mintchev, Baalasubramanian, Sivasankar, Pickering, Matthew C., Wu, Xiaobo, Harris, Claire Louise and Morgan, Bryan Paul ORCID: 2009. Crry deficiency in complement sufficient mice: C3 consumption occurs without associated renal injury. Molecular Immunology 46 (5) , pp. 803-811. 10.1016/j.molimm.2008.09.003

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The rodent-specific complement regulator complement receptor 1-related gene/protein-y (Crry) is critical for complement homeostasis. Gene deletion is 100% embryonically lethal; Crry-deficient (Crry(-/-)) mice were rescued by back-crossing onto C3 deficiency, confirming that embryo loss was complement mediated. In order to rescue viable Crry(-/-) mice without deleting C3, we have tested inhibition of C5 during gestation. Crry(+/-) females were given neutralizing anti-C5 mAb immediately prior to mating with Crry(+/-) males and C5 inhibition maintained through pregnancy. A single, healthy Crry(-/-) female was obtained and mating with Crry(+/-) males yielded healthy litters containing equal numbers of Crry(+/-) and Crry(-/-) pups. Inter-crossing Crry(-/-) mice yielded healthy litters of expected size. Although the mice were not anemic, exposure of Crry(-/-) erythrocytes to normal mouse serum caused C3 deposition and lysis, while transfusion into normal or C6(-/-) mice resulted in rapid clearance. Complement activity and C3 levels in Crry(-/-) mice were markedly reduced. Comparison with factor H deficient (CfH(-/-)) mice revealed similar levels of residual C3; however, unlike the CfH(-/-) mice, Crry(-/-) mice showed no evidence of renal injury, demonstrating distinct roles for these regulators in protecting the kidney.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Subjects: R Medicine > R Medicine (General)
Uncontrolled Keywords: Complement; Crry; Knockout; Mouse
Publisher: Elsevier
ISSN: 0161-5890
Last Modified: 06 Dec 2022 09:40

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