FcγRIIB as a modulator of autoimmune disease susceptibility

Abstract

Antibodies are secreted to recognize and in some cases directly neutralize pathogens. Another important means by which they are essential components of the immune system is through binding to Fc receptors. Effector responses triggered by antibody binding of Fc receptors affect a host of important cellular responses such as phagocytosis, inflammatory cytokine release, antigen presentation, and regulation of humoral responses. A crucial check on this antibody-mediated signal is through the inhibitory receptor, FcγRIIB. In this review we discuss how dysregulation of FcγRIIB can result in a lowered threshold for autoimmunity in mice and humans. We close with a discussion of the potential for applying these findings to immunotherapy.

• SLE, susceptibility
• Fc gamma receptors (FcγR)
• FcγRIIB

Acknowledgements

We would like to thank other members of the Autoimmunity and Functional Genomics Section for thoughtful discussions. This work is supported by the NIH Intramural Research Program.