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.