Abstract
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 language | English |
|---|---|
| Pages (from-to) | 105-112 |
| Number of pages | 8 |
| Journal | American Journal of Respiratory and Critical Care Medicine |
| Volume | 169 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 1 2004 |
| Externally published | Yes |
Keywords
- Eosinophil
- Fc receptor
- IgE
- Mouse
- Rhinitis
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine