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

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  • Azusa Ujike
    From the *Department of Experimental Immunology and the ‡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
  • Yoko Ishikawa
    From the *Department of Experimental Immunology and the ‡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
  • Masao Ono
    From the *Department of Experimental Immunology and the ‡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
  • Takae Yuasa
    From the *Department of Experimental Immunology and the ‡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
  • Tadashi Yoshino
    From the *Department of Experimental Immunology and the ‡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
  • Manabu Fukumoto
    From the *Department of Experimental Immunology and the ‡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
  • Jeffrey V. Ravetch
    From the *Department of Experimental Immunology and the ‡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
  • Toshiyuki Takai
    From the *Department of Experimental Immunology and the ‡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

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<jats:p>It is widely accepted that immunoglobulin (Ig)E triggers immediate hypersensitivity responses by activating a cognate high-affinity receptor, FcεRI, 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, FcγRII and III. We have addressed the in vivo significance of this interaction by studying IgE-mediated passive systemic anaphylaxis in FcγR-deficient mice. Mice deficient in the inhibitory receptor for IgG, FcγRIIB, display enhanced IgE-mediated anaphylactic responses, whereas mice deficient in an IgG activation receptor, FcγRIII, display a corresponding attenuation of IgE-mediated responses. Thus, in addition to modulating IgG-triggered hypersensitivity responses, FcγRII 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.</jats:p>

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