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Updated: Jul 29, 2026
12:04
The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Receptor revision and systemic lupus
1Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, USA.
Scandinavian Journal of Immunology
|April 27, 2002
Summary
B cells use receptor editing to prevent self-reactivity, but defects in this process are linked to autoimmune diseases like lupus. Abnormalities in B cell editing may contribute to lupus development.
Area of Science:
- Immunology
- Molecular Biology
- Autoimmunity
Background:
- B cells can undergo secondary immunoglobulin rearrangements, a process called receptor editing, during development.
- Receptor editing is crucial for maintaining self-tolerance by eliminating self-reactive B cells in the bone marrow.
- The role of receptor editing in peripheral immune responses is still under investigation.
Purpose of the Study:
- To explore the role of receptor editing in B cell development and immune responses.
- To investigate the abnormalities in receptor editing observed in patients with systemic autoimmune diseases, such as lupus.
- To determine if lupus-associated editing defects are a cause or consequence of the disease.
Main Methods:
- Review of studies on B cell receptor editing over the past 10 years.
- Analysis of B cell development and tolerance mechanisms in both normal and autoimmune conditions.
- Examination of the link between receptor editing defects and autoantibody production.
Main Results:
- Receptor editing is essential for eliminating self-reactive B cells, preventing autoimmunity.
- Abnormalities in receptor editing are evident in systemic autoimmune diseases like lupus.
- Both decreased and excessive receptor editing can contribute to the development of autoimmunity.
Conclusions:
- Defects in B cell receptor editing are intricately linked to systemic autoimmune diseases, particularly lupus.
- Altered receptor editing may lead to the persistence of self-reactive B cells or the production of autoantibodies.
- Further research is needed to clarify whether lupus-associated editing defects are a primary cause or a secondary consequence of the disease.
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