IgE antibodies, when cross-linked by allergen on the surface of effect
or cells such as mast cells and basophils, are known to be directly re
sponsible for immediate type hypersensitivity reactions. In addition,
IgE may be involved in other, indirect, mechanisms, fundamental to the
pathogenesis of allergic diseases, such as enhancement of the antigen
capturing capacity of antigen presenting cells. IgE mediated antigen
presentation could lead to a continuous activation of the immune syste
m by very low concentrations of allergen. As a result, Th2 cell popula
tions may expand and may induce more B cells to switch to IgE producti
on. Subsequently, the overproduction of IgE and Th2 cells in a patient
may explain the clinical observation that certain allergic patients d
eteriorate from sensitivity to a single group of allergens to sensitiv
ity to multiple groups of allergens. Therefore, control of IgE product
ion is not only important for the treatment of allergic symptoms, but
may also regulate deterioration of allergy via the mechanism of CD23/I
gE mediated allergen presentation by naive B cells. The role that mono
cytes, which have recently been found to express Fc epsilon RI, play i
n the pathogenesis of allergy, remains speculative. We hypothesize tha
t their role may be to remove IgE from the circulation and re-direct t
he immune response from naive B cells. IgG antibodies which cannot be
used for antigen uptake by B cells also direct the immune response to
monocytes.