1. Introduction
Allergic diseases are a rising global health threat and economic burden(1–3). In classical type I hypersensitivity, Immunoglobulin E (IgE) is the key molecule in the development of allergic reactions towards allergens (4,5). Specific IgE reacting with allergens triggers the release of inflammatory mediators through allergen-mediated cross-linking of the high affinity receptor, FcεRI on allergic effector cells such as mast cells and basophils(6–8).
The second IgE receptor CD23 (FcεRII) has largely been overlooked as a potentially important molecule in the field of allergy research (9). This is possibly the case because CD23 is involved in a complex variety of different immunological processes (10). Besides its role as an IgE receptor, CD23 has been shown to play a role in the development and growth of normal and leukemic B cells (11,12). Furthermore, it has been studied as a C-type lectin where it was shown to facilitate antimicrobial immunity (13–17) and can even be engaged by sialylated IgG to act as a Fcγ receptor( 18–20). Apart from its form as a membrane receptor, CD23 can be cleaved into soluble fragments (sCD23) which has been studied as a disease marker in allergy, rheumatoid arthritis and leukemia (21–24). Furthermore, sCD23 has been shown to activate monocytes via CD11b and CD11c integrins (25–27).
Here, we focus on CD23 as an IgE receptor, particularly in the allergic context where CD23 acts as a regulator of IgE levels and modulator of immune responses. Even though the book on CD23 is still far from closed, several recent findings have shed light on the function of CD23 and show that CD23 could become a key molecule to investigate current treatment options in allergy and to develop novel strategies.