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A role for CD23 in the suppression of allergy
  • Monique Vogel,
  • Paul Engeroff
Monique Vogel
Inselspital University Hospital Berne Institute of Immunology
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Paul Engeroff
Inselspital University Hospital Berne Institute of Immunology
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Abstract

IgE, the key molecule in atopy has been shown to bind two receptors, FcRI, the high affinity receptor and FcεRII (CD23), mostly found on B cells and that binds IgE with lower affinity. Whereas cross-linking of IgE on FcRI triggers allergic reaction, binding of IgE to CD23 is known to play an important role in both IgE synthesis and presentation. Thus, targeting IgE-immune complexes on B cells has shown to 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 matter of debate. Here, we discuss several mechanisms related to IgE and IgE binding to both receptors, as well as the influence of the antigen binding on different immune cells expressing the receptors. One recent paper has shown that free IgE preferentially binds to FcRI whereas IgE immune complexes (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 the antigen presentation by delivering antigen to dendritic cells. The data suggest that CD23 play a multifunctional role in regulating the allergic response pathway.

Peer review status:ACCEPTED

06 Oct 2020Submitted to Allergy
06 Oct 2020Submission Checks Completed
06 Oct 2020Assigned to Editor
11 Oct 2020Reviewer(s) Assigned
26 Oct 2020Review(s) Completed, Editorial Evaluation Pending
26 Oct 2020Editorial Decision: Revise Minor
14 Dec 20201st Revision Received
15 Dec 2020Submission Checks Completed
15 Dec 2020Assigned to Editor
15 Dec 2020Reviewer(s) Assigned
22 Dec 2020Review(s) Completed, Editorial Evaluation Pending
22 Dec 2020Editorial Decision: Accept