B Cell Receptor Signaling in Human Systemic Lupus Erythematosus

Aimee E. Pugh-Bernard; John C. Cambier

Disclosures

Curr Opin Rheumatol. 2006;18(5):451-455. 

In This Article

Conclusion

Although research addressing the contribution of B cell defects in SLE has been quite fruitful, the data accumulated thus far do not indicate that a single B cell defect contributes to SLE. Abnormal B cell signaling and hyperactivity is an aspect of both murine and human lupus that certainly plays a significant role in the breakdown of B cell tolerance and the subsequent pathogenesis of SLE. Recent work has shown that deficient FcγRIIB-mediated suppression of BCR signaling contributes to the increased calcium response and hyperactivity observed in human SLE B cells. Decreased Lyn expression may also contribute to the characteristic hyperactivity of SLE B cells. Increased levels of BAFF may influence the escape of B cell tolerance to dsDNA resulting in the production of anti-dsDNA antibodies. Combined, the research to date suggests that B cell hyperactivity due to multiple signaling abnormalities most likely plays a central role in the development of disease.

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