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Updated: Apr 29, 2026
The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
Published on: November 1, 2015
The complement system in systemic lupus erythematosus: an update
Jonatan Leffler1, Anders A Bengtsson2, Anna M Blom3
1Division of Medical Protein Chemistry, Department of Laboratory Medicine Malmö, Lund University, Malmö, Sweden Division of Cell Biology and Immunology, Telethon Kids Institute, University of Western Australia, Subiaco, Australia.
Insights
The complement system
Area of Science:
- Immunology and Rheumatology
- Autoimmune Disease Research
Background:
- The complement system is integral to the immune response but has a complex role in systemic lupus erythematosus (SLE), potentially both protecting against and worsening the disease.
- Genetic factors, including C1q deficiency and mutations in complement receptors and inhibitors, are linked to SLE development and severity.
- Autoantibodies are key to SLE pathogenesis, and the complement system's influence on adaptive immunity is a critical area of study.
Purpose of the Study:
- To review recent advancements in understanding the complement system's role in systemic lupus erythematosus (SLE) pathogenesis.
- To highlight the dual role of complement in SLE, encompassing both protective and detrimental effects.
- To explore the diagnostic and monitoring potential of complement biomarkers in SLE.
Main Methods:
- Literature review of recent complement-focused research in SLE.
- Analysis of genetic associations with complement components and receptors in SLE patients.
- Examination of complement's impact on SLE-specific manifestations and autoantibody production.
Main Results:
- C1q deficiency, though rare, is a significant genetic risk factor for SLE.
- New genetic associations with complement receptors and inhibitors indicate their involvement in SLE onset and nephritis.
- Complement contributes to SLE manifestations like glomerulonephritis and thrombosis, and influences autoantibody responses.
- Complement components in plasma show potential as accessible biomarkers for SLE diagnosis and activity monitoring.
Conclusions:
- The complement system is a critical player in SLE pathogenesis, with complex and multifaceted roles.
- Recent genetic discoveries and insights into complement's influence on immune responses deepen our understanding of SLE.
- Complement's accessibility in plasma positions it as a promising avenue for SLE biomarker development and disease management.
Abstract:
The complement system plays a major role in the autoimmune disease, systemic lupus erythematosus (SLE). However, the role of complement in SLE is complex since it may both prevent and exacerbate the disease. In this review, we explore the latest findings in complement-focused research in SLE. C1q deficiency is the strongest genetic risk factor for SLE, although such deficiency is very rare. Various recently discovered genetic associations include mutations in the complement receptors 2 and 3 as well as complement inhibitors, the latter related to earlier onset of nephritis. Further, autoantibodies are a distinct feature of SLE that are produced as the result of an adaptive immune response and how complement can affect that response is also being reviewed. SLE generates numerous disease manifestations involving contributions from complement such as glomerulonephritis and the increased risk of thrombosis. Furthermore, since most of the complement system is present in plasma, complement is very accessible and may be suitable as biomarker for diagnosis or monitoring of disease activity. This review highlights the many roles of complement for SLE pathogenesis and how research has progressed during recent years.
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