The binding of IgE to high-affinity IgE receptors (Fc epsilon RI) on t
he surface of mast cells and basophils primes these cells to secrete a
panel of proinflammatory mediators upon subsequent exposure to specif
ic Ag. We now find that the level of Fc epsilon RI expression on bone
marrow basophils in mice infected with the nematode Strongyloides vene
zuelensis exhibits a strong positive correlation with the serum concen
tration of IgE, as was previously reported for human blood basophils.
Moreover, the administration of IgE in vivo can significantly up-regul
ate Fc epsilon RI expression on mouse basophils, and genetically IgE-d
eficient (IgE -/-) mice exhibit a dramatic (similar to 81%) reduction
of basophil Fc epsilon RI expression compared with the corresponding n
ormal (IgE +/+) mice. The finding that IgE can be a major regulator of
mouse basophil Fc epsilon RI expression in vivo identifies a potentia
lly important mechanism for enhancing the expression of effector cell
function in IgE-dependent allergic reactions or immunologic responses
to parasites.