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Defective B cell tolerance checkpoints in systemic lupus erythematosus
Sergey Yurasov1, Hedda Wardemann, Johanna Hammersen
1Laboratory of Molecular Immunology, The Rockefeller University, New York, NY, USA.
The Journal of Experimental Medicine
|March 2, 2005
Summary
Systemic lupus erythematosus (SLE) involves a breakdown in immune tolerance, leading to self-reactive antibodies. This study reveals defective early B cell tolerance checkpoints in adolescent SLE patients, allowing self-reactive B cells to persist.
Area of Science:
- Immunology
- Autoimmunity
- B cell biology
Background:
- Systemic lupus erythematosus (SLE) is characterized by autoantibodies, indicating a breakdown in immune tolerance.
- Self-reactive antibodies in SLE precede clinical symptoms, but the precise point of tolerance breakdown in B cell development remains unclear.
Purpose of the Study:
- To investigate the early B cell development checkpoints responsible for maintaining immune tolerance in patients with SLE.
- To determine if defects in these early checkpoints contribute to the autoantibody production observed in SLE.
Main Methods:
- Analysis of B cell development checkpoints in three adolescent patients diagnosed with SLE.
- Quantification of self-reactive antibodies in mature naive B cells from SLE patients and healthy controls.
Main Results:
- Defects were identified in two discrete early checkpoints of B cell development in the adolescent SLE patients.
- A significantly higher proportion of mature naive B cells (25-50%) produced self-reactive antibodies in SLE patients compared to controls (5-20%).
Conclusions:
- Early B cell tolerance mechanisms are abnormal in systemic lupus erythematosus.
- Defective early B cell tolerance checkpoints may be a key factor in the development of autoantibodies in SLE.
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