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J. Exp. Med.,
Volume 189, Number 10, May 17, 1999 1573-1579
By
From the * Department of Experimental Immunology and the It is widely accepted that immunoglobulin (Ig)E triggers immediate hypersensitivity responses
by activating a cognate high-affinity receptor, Fc Department of Pathology, Institute of
Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan; § Core Research for
Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST),
Tokyo 101-0062, Japan; Second Department of Pathology, Okayama University Medical School,
Okayama 700-8558, Japan; and ¶ Laboratory of Molecular Genetics and Immunology, The
Rockefeller University, New York 10021
RI, leading to mast cell degranulation with
release of vasoactive and proinflammatory mediators. This apparent specificity, however, is
complicated by the ability of IgE to bind with low affinity to Fc receptors for IgG, Fc
RII and
III. We have addressed the in vivo significance of this interaction by studying IgE-mediated passive systemic anaphylaxis in FcR-deficient mice. Mice deficient in the inhibitory receptor
for IgG, FcRIIB, display enhanced IgE-mediated anaphylactic responses, whereas mice deficient in an IgG activation receptor, FcRIII, display a corresponding attenuation of IgE-mediated responses. Thus, in addition to modulating IgG-triggered hypersensitivity responses, FcRII
and III on mast cells are potent regulators of IgE-mediated responses and reveal the existence of
a regulatory pathway for IgE triggering of effector cells through IgG Fc receptors that could
contribute to the etiology of the atopic response.
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