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. [ABSTRACT FROM AUTHOR]
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