Immunoglobulin E (
IgE)-mediated
allergy is the most common
hypersensitivity disease affecting more than 30% of the population. Exposure to even minute quantities of
allergens can lead to the production of
IgE antibodies in atopic individuals. This is termed allergic sensitization, which occurs mainly in early childhood.
Allergen-specific
IgE then binds to the high (FcεRI) and low-affinity receptors (FcεRII, also called CD23) for
IgE on effector cells and antigen-presenting cells. Subsequent and repeated
allergen exposure increases
allergen-specific
IgE levels and, by receptor cross-linking, triggers immediate release of inflammatory mediators from mast cells and basophils whereas
IgE-facilitated
allergen presentation perpetuates T cell-mediated allergic
inflammation. Due to engagement of receptors which are highly selective for
IgE, even tiny amounts of
allergens can induce massive
inflammation. Naturally occurring
allergen-specific
IgG and
IgA antibodies usually recognize different
epitopes on
allergens compared with
IgE and do not efficiently interfere with
allergen-induced
inflammation. However,
IgG and
IgA antibodies to these important
IgE epitopes can be induced by
allergen-specific
immunotherapy or by passive immunization. These will lead to competition with
IgE for binding with the
allergen and prevent allergic responses. Similarly,
anti-IgE treatment does the same by preventing
IgE from binding to its receptor on mast cells and basophils. Here, we review the complex interplay of
allergen-specific
IgE,
IgG and
IgA and the corresponding cell receptors in allergic diseases and its relevance for diagnosis, treatment and prevention of
allergy.