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RI1
*
Department of Pathology, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, MA 02215; and
Department of Dermatology, Johns Hopkins Hospital, Baltimore, MD 21205
The IgE-Fc
RI network plays a central role in allergic
inflammation. IgE levels control cell surface levels of FcRI and, in
turn, FcRI levels modulate the intensity of effector responses.
Treatment of allergic patients with anti-IgE Abs has been shown to
induce a decrease in FcRI expression on basophils and a decrease in
Ag-triggered histamine release. However, the mechanisms underlying
IgE-mediated regulation of FcRI expression remain unclear. Here, we
designed an in vitro model system to establish the minimal cellular
requirements for regulation of FcRI by IgE. Using this system, we
demonstrate that transcriptional regulation, hemopoietic-specific
factors, and signaling are not required for IgE-mediated increases in
FcRI expression. IgE binding to the 
-chain is the minimal
requirement for the induction of FcRI up-regulation. The rate of
up-regulation is independent of the baseline level of expression. The
mechanism of this up-regulation is the result of a combination of three
factors: 1) stabilization of the receptor at the cell surface, which
prevents receptor internalization and degradation; 2) use of a
preformed pool of receptor comprising recycled and recently synthesized
receptors; and 3) continued basal level of protein synthesis. It is
possible that in vivo additional factors contribute to modulate the
basic regulatory mechanism described here.
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