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

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<jats:p> <jats:bold>Background:</jats:bold> Interleukin (IL)‐4 is believed to play an important role in the atopic pathogenesis. However, the precise role of IL‐4 in the <jats:italic>in vivo</jats:italic> initiation of allergic rhinitis is not fully understood. We have recently found that BALB/c mice sensitized intranasally with <jats:italic>Schistosoma mansoni</jats:italic> 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 <jats:italic>in vivo</jats:italic> with this model.</jats:p><jats:p> <jats:bold>Methods:</jats:bold> 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 <jats:italic>in vivo</jats:italic> and <jats:italic>in vitro</jats:italic>.</jats:p><jats:p> <jats:bold>Results:</jats:bold> 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.</jats:p><jats:p> <jats:bold>Conclusions:</jats:bold> 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.</jats:p>

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  • Allergy

    Allergy 55 (8), 723-731, 2000-08

    Wiley

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