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Targeted disruption of the murine gene coding for the third complement component (C3)
M Pekna1, M A Hietala, T Rosklint
1Department of Medical Biochemistry, University of Göteborg, Sweden.
Insights
Researchers created mice lacking the third complement component (C3). These mice, unable to activate complement, offer a new model for studying the complement system's role in health and disease.
Area of Science:
- Immunology
- Biochemistry
Background:
- The complement system comprises over 30 plasma and cell membrane proteins.
- It plays crucial roles in immunity, including inflammation, pathogen elimination, and immune complex clearance.
- Dysregulated complement activation is implicated in various diseases, such as autoimmune disorders and atherosclerosis.
Purpose of the Study:
- To generate a novel animal model for investigating the in vivo functions of the complement system.
- To create mice deficient in the third complement component (C3) to block complement activation early.
Main Methods:
- Gene targeting was employed to create C3-deficient mice.
- This deficiency prevents complement activation via all known pathways.
Main Results:
- Successfully generated mice lacking the third complement component (C3).
- These mice serve as a model with inhibited early-stage complement activation.
Conclusions:
- C3-deficient mice provide a valuable tool for in vivo research on the complement system.
- This model will aid in understanding complement's role in diverse physiological and pathological contexts.
Abstract:
Complement is a system of more than 30 proteins found both in plasma and on cell membranes. The complement system has several important functions in the immune response including initiation of inflammation, neutralization and elimination of pathogens, regulation of antibody responses, clearance of immune complexes and disruption of cell membranes. Under certain conditions complement may, however, act as a mediator of deleterious inflammatory reactions and complement activation has been implicated in the pathogenesis of autoimmune disorders, atherosclerosis, neurodegenerative diseases, bioincompatibility reactions and decompression sickness. Using gene targeting, we have generated mice deficient for the third complement component (C3). These mice represent an animal model in which complement activation by any pathway is prevented at an early stage. The C3-deficient mice should be valuable for the study of the roles of the complement system in vivo in a variety of physiological and pathological situations.