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Published on: August 19, 2014
Modulation of peripheral B cell tolerance by CD72 in a murine model
Daniel Hsieh-Hsin Li1, Monte M Winslow, Thai M Cao
1Stanford University School of Medicine, Stanford, California 94305, USA. dhli70x7@gmail.com
Arthritis and Rheumatism
|September 30, 2008
Summary
CD72 is crucial for maintaining B cell tolerance and preventing autoimmune diseases like lupus. Its absence leads to B cells improperly responding to self-antigens, causing autoantibody production.
Area of Science:
- Immunology
- Autoimmunity
- Molecular Biology
Background:
- B cells are key players in autoimmune diseases such as systemic lupus erythematosus.
- The precise mechanisms by which B cell signaling contributes to autoantibody production are not fully understood.
Purpose of the Study:
- To investigate the role of CD72 in regulating B cell receptor (BCR)-mediated signaling.
- To determine CD72's function in maintaining peripheral B cell tolerance.
Main Methods:
- Utilized a mouse model with hen egg lysozyme (HEL)
- anergic
- B cells.
- Generated CD72-deficient mice and analyzed B cell signaling pathways.
- Examined aged wild-type and CD72-deficient mice for autoimmune manifestations.
Main Results:
- CD72 deficiency resulted in inappropriate proliferation and survival of anergic B cells upon self-antigen stimulation.
- CD72 was found to down-regulate BCR signaling, limiting calcium influx and activation of key signaling molecules (NFATc1, NF-kappaB, MAPK, Akt).
- CD72 interacts with the adaptor molecule Cbl-b, suggesting a mechanism for its negative regulatory role.
- Aged CD72-deficient mice exhibited spontaneous autoantibody production and lupus-like disease features.
Conclusions:
- CD72 is essential for maintaining B cell anergy and peripheral tolerance.
- Dysregulation of CD72 may contribute to the pathogenesis of systemic lupus erythematosus.
