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

Ruseva, Marieta Milkova, Hughes, Timothy Richard, Donev, Rossen Mintchev, Baalasubramanian, Sivasankar, Pickering, Matthew C., Wu, Xiaobo, Harris, Claire Louise and Morgan, Bryan Paul 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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Abstract

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: 07 Feb 2019 21:37
URI: http://orca-mwe.cf.ac.uk/id/eprint/25501

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