Increased serum C3 levels in Crry transgenic mice partially abrogates its complement inhibitory effects
1Department of Laboratory Medicine, Hallym University College of Medicine, Anyang, Korea. kangheejung@hallym.or.kr
Clinical and Experimental Immunology
|April 17, 2004
Summary
Complement receptor 1-related gene/protein y (Crry) is a complement regulator. In transgenic mice, increased C3 levels compensated for soluble Crry
Area of Science:
- Immunology
- Complement System Biology
Background:
- Complement receptor 1-related gene/protein y (Crry) is a potent murine complement regulator.
- Transgenic mice overexpressing soluble Crry (sCrry) are models for chronic complement activation blockade.
Purpose of the Study:
- To elucidate the mechanism behind unexpected alternative pathway (AP) activity in Crry transgenic mice.
- To evaluate AP activities and complement component levels in transgenic and non-transgenic mice.
Main Methods:
- Induction of sCrry expression in transgenic mice by zinc sulphate feeding.
- Measurement of AP activity, sCrry levels, and complement components (C3, factor B, H, D) in serum.
- Immunoprecipitation and removal of sCrry to assess its functionality.
Main Results:
- sCrry was expressed at significant levels (70.1 ± 42.7 μg/ml) but did not decrease AP activity compared to controls.
- Expressed sCrry was functional, as its removal enhanced AP activity.
- Serum C3 levels were significantly increased in transgenic mice after zinc feeding (142.8 ± 14.1% vs. 121.4 ± 15.1%).
Conclusions:
- The inhibitory effect of chronic sCrry exposure is compensated by increased C3 levels.
- A complement regulatory protein likely controls serum C3 levels, impacting complement inhibitor studies.
