The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/5/1573/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 10, May 17, 1999 1573-1579

Articles

Modulation of Immunoglobulin (Ig)E-mediated Systemic Anaphylaxis by Low-Affinity Fc Receptors for IgG

Azusa Ujike*,§, Yoko Ishikawa*, Masao Ono*,§, Takae Yuasa*,§, Tadashi Yoshino||, Manabu Fukumoto{ddagger}, Jeffrey V. Ravetch, and Toshiyuki Takai*,§

From the * Department of Experimental Immunology and the {ddagger} 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

It is widely accepted that immunoglobulin (Ig)E triggers immediate hypersensitivity responses by activating a cognate high-affinity receptor, Fc{varepsilon}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{gamma}RII and III. We have addressed the in vivo significance of this interaction by studying IgE-mediated passive systemic anaphylaxis in Fc{gamma}R-deficient mice. Mice deficient in the inhibitory receptor for IgG, Fc{gamma}RIIB, display enhanced IgE-mediated anaphylactic responses, whereas mice deficient in an IgG activation receptor, Fc{gamma}RIII, display a corresponding attenuation of IgE-mediated responses. Thus, in addition to modulating IgG-triggered hypersensitivity responses, Fc{gamma}RII 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.

Key Words: systemic anaphylaxis • Fc receptor • immunoglobulin E • mast cell • gene targeting

Address correspondence to Toshiyuki Takai, Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo, Sendai 980-8575, Japan. Phone: 81-22-717-8501; Fax: 81-22-717-8505; E-mail: tostakai{at}idac.tohoku.ac.jp

Abbreviations used: BMMC, bone marrow–derived cultured mast cells; Fc{varepsilon}RI, high-affinity receptor for IgE; Fc{gamma}R, Fc receptor for IgG; FcR{gamma}, Fc receptor {gamma} subunit; Fc{gamma}RIIB and Fc{gamma}RIII, type IIB and type III low-affinity receptors for IgG, respectively.


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