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

Mol. Immunol.2009 Feb;46(5):803-11. Epub 2008 Oct 22
Marieta M Ruseva 1 , Timothy R Hughes , Rossen M Donev , Baalasubramanian Sivasankar , Matthew C Pickering , Xiaobo Wu , Claire L Harris , B Paul Morgan
Marieta M Ruseva 1 , Timothy R Hughes , Rossen M Donev , Baalasubramanian Sivasankar , Matthew C Pickering , Xiaobo Wu , Claire L Harris , B Paul Morgan
+ et al

[No authors listed]

Author information
  • 1 Complement Biology Group, Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK.

摘要


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.