The role of CD23 in the regulation of allergic responses

IgE, the key molecule in atopy has been shown to bind two receptors, Fc epsilon RI, the high-affinity receptor, and Fc epsilon RII (CD23), binding IgE with lower affinity. Whereas cross-linking of IgE on Fc epsilon RI expressed by mast cells and basophils triggers the allergic reaction, binding of IgE to CD23 on B cells plays an important role in both IgE regulation and presentation. Furthermore, IgE-immune complexes (IgE-ICs) bound by B cells enhance antibody and T cell responses in mice and humans. However, the mechanisms that regulate the targeting of the two receptors and the respective function of the two pathways in inflammation or homeostasis are still a matter of debate. Here, we focus on CD23 and discuss several mechanisms related to IgE binding, as well as the impact of the IgE/antigen-binding on different immune cells expressing CD23. One recent paper has shown that free IgE preferentially binds to Fc epsilon RI whereas IgE-ICs are preferentially captured by CD23. Binding of IgE-ICs to CD23 on B cells can, on one hand, regulate serum IgE and prevent effector cell activation and on the other hand facilitate antigen presentation by delivering the antigen to dendritic cells. These data argue for a multifunctional role of CD23 for modulating IgE serum levels and immune responses.

Automated summary

IgE can bind to two receptors, playing different roles on different cells, inducing allergic reactions on one hand and participating in IgE regulation and antigen presentation on the other. In inflammation and immune homeostasis, CD23 plays an important modulatory role.