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, Jeffrey V. Ravetch, Toshiyuki Takai

Research output: Contribution to journalArticlepeer-review

158 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1573-1579
Number of pages7
JournalJournal of Experimental Medicine
Issue number10
Publication statusPublished - May 17 1999
Externally publishedYes


  • Fc receptor
  • Gene targeting
  • Immunoglobulin E
  • Mast cell
  • Systemic anaphylaxis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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