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Published ahead of print on October 2, 2003, doi:10.1164/rccm.200302-239OC

Am. J. Respir. Crit. Care Med., Volume 169, Number 1, January 2004, 105-112

A more recent version of this article appeared on January 1, 2004
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Submitted on February 20, 2003
Accepted on September 25, 2003

Roles of FcgRIIB in nasal eosinophilia and IgE production in murine allergic rhinitis

Tohru Watanabe1, Mitsuhiro Okano1*, Hisashi Hattori1, Tadashi Yoshino2, Nobuaki Ohno3, Nobuo Ohta4, Yuji Sugata1, Yorihisa Orita1, Toshiyuki Takai5, and Kazunori Nishizaki1

1 Otolaryngology - Head and Neck Surgery, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan, 2 Pathology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan, 3 Otolaryngology, Nagoya City University Medical School, Nagoya, Aichi, Japan, 4 Medical Zoology, Nagoya City University Medical School, Nagoya, Aichi, Japan, 5 Experimental Immunology, Institute of Development, Aging and Cancer, Sendai, Miyagi, Japan

* To whom correspondence should be addressed. E-mail: mokano{at}cc.okayama-u.ac.jp.

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




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