Roles of FcγRIIB in Nasal Eosinophilia and IgE Production in Murine Allergic Rhinitis

Tohru Watanabe, Mitsuhiro Okano, Hisashi Hattori, Tadashi Yoshino, Nobuaki Ohno, Nobuo Ohta, Yuji Sugata, Yorihisa Orita, Toshiyuki Takai, Kazunori Nishizaki

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)


The low-affinity IgG Fc receptor, FcγRIIB, displays inhibitory potential in experimental models such as autoimmune diseases. However, whether this receptor is involved in the onset of allergic diseases remains unknown. This study examines the role of FcγRIIB in the initiation of allergic rhinitis in mice. Repeated intranasal sensitizatlon with Schistosoma mansoni egg antigen (SEA) induced SEA-specific IgE and marked nasal eosinophilia in high-responder BALB/ c mice. FcγRIIB gene-deficient (-/-) BALB/c mice displayed severe eosinophilia compared with that of wild-type counterparts. However, FcγRIIB -/- mice conversely produced less SEA-specific IgE. The production of interleukin (IL)-4 but not of IL-5 or IFN-γ by nasal mononuclear cells was also decreased in FcγRIIB -/- mice, suggesting that the exacerbation of nasal eosinophila in FcyRIIB -/- mice is independent of the local IL-5 levels. The findings in low responder C57BL/6 mice were similar. In addition, nasal eosinophilia in FcγRIIB -/- mice passively sensitized with SEA was exacerbated, and conversely, specific IgE production was inhibited after a nasal challenge. These results suggest that FcγRIIB plays a regulatory role in the initiation of allergic rhinitis that is independent of either mouse strain or type of sensitization.

Original languageEnglish
Pages (from-to)105-112
Number of pages8
JournalAmerican Journal of Respiratory and Critical Care Medicine
Issue number1
Publication statusPublished - Jan 1 2004
Externally publishedYes


  • Eosinophil
  • Fc receptor
  • IgE
  • Mouse
  • Rhinitis

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine


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