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Effects of decomplementation with cobra venom factor on experimental vasculitis
P W Mathieson1, F J Qasim, S Thiru
1Department of Medicine Unit, University of Cambridge, UK.
Clinical and Experimental Immunology
|September 1, 1994
Summary
Mercuric chloride induces autoimmunity and tissue injury. Complement depletion did not affect autoantibody levels but worsened injury when administered mid-course, suggesting a role for complement activation products.
Area of Science:
- Immunology
- Toxicology
- Pathology
Background:
- Mercuric chloride (HgCl2) is a known inducer of autoimmunity in susceptible rats.
- This model is characterized by hyper-immunoglobulin E (IgE), autoantibodies, and tissue damage, including necrotizing vasculitis.
- The early phase involves granulocyte infiltration, followed by immunoglobulin deposition.
Purpose of the Study:
- To investigate the role of the complement system in HgCl2-induced autoimmunity.
- To determine if complement activation is essential for autoantibody production or tissue injury.
Main Methods:
- Rats were treated with HgCl2 over 10 days.
- Cobra venom factor (CVF) was administered at different time points (day 0, 5, or 10) to induce transient decomplementation.
- Serum IgE, autoantibody levels, and tissue injury were assessed.
Main Results:
- Serum IgE and autoantibody levels were comparable across all groups, regardless of CVF administration timing.
- Tissue injury was not significantly altered in rats receiving CVF early or late in the HgCl2 treatment course.
- Administration of CVF at an intermediate time point (day 5) significantly exacerbated tissue injury compared to controls.
Conclusions:
- The complement system does not appear to play a major role in the induction of autoantibodies by HgCl2.
- Complement is not essential for the effector phase of HgCl2-induced tissue injury.
- Exacerbation of injury in the intermediate CVF group may be due to pro-inflammatory complement activation products during active granulocyte-mediated damage.