Interleukin‐4‐independent production of Th2 cytokines by nasal lymphocytes and nasal eosinophilia in murine allergic rhinitis

Background: Interleukin (IL)‐4 is believed to play an important role in the atopic pathogenesis. However, the precise role of IL‐4 in the in vivo initiation of allergic rhinitis is not fully understood. We have recently found that BALB/c mice sensitized intranasally with Schistosoma mansoni egg antigen (SEA) mount a Th2 response that initiates allergic rhinitis. Thus, we sought to determine the role of IL‐4 in the initiation of allergic rhinitis in vivo with this model. Methods: IL‐4 gene‐deficient (IL‐4−/−) BALB/c and wild‐type (IL‐4+/+) control mice were sensitized by intranasal SEA administration, and their immunologic responses were examined both in vivo and in vitro . Results: IL‐4+/+ mice sensitized with SEA displayed significantly higher titers of SEA‐specific IgG1 and IgE antibodies than IL‐4−/− mice, while the latter produced significantly more SEA‐specific IgG2a. Antigen‐stimulated nasal lymphocytes from SEA‐sensitized IL‐4−/− and IL‐4+/+ mice produced similar amounts of IL‐5 and IL‐10, but neither produced IFN‐γ. Furthermore, the severity of nasal eosinophilia was similar in both groups. Conclusions: These results indicate that although IL‐4 is necessary for the production of Th2‐associated antibodies – in particular, IgE – it is not required for either the production of the Th2‐associated cytokines IL‐5 and IL‐10, or the induction of nasal eosinophilia.