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

Abstract

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. 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. 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-gamma. Furthermore, the severity of nasal eosinophilia was similar in both groups. 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.