1. IL-33, but Not IL-25, Is Crucial for the Development of House Dust Mite Antigen-Induced Allergic Rhinitis
- Author
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Tatuya Yamasoba, Kenji Matsumoto, Kenji Kondo, Hirohisa Saito, Wakako Nakanishi, Maho Suzukawa, Hajime Suto, Akira Matsuda, Susumu Nakae, Akiko Shibui, Sachiko Yamaguchi, and Aya Nambu
- Subjects
Male ,Rhinitis, Allergic, Perennial ,Science ,Mucous membrane of nose ,Mice ,medicine ,Animals ,Antigens, Dermatophagoides ,House dust mite ,Goblet cell ,Multidisciplinary ,biology ,Interleukins ,Interleukin-17 ,Pyroglyphidae ,Interleukin ,Eosinophil ,biology.organism_classification ,Interleukin-33 ,Rhinitis, Allergic ,Interleukin 33 ,medicine.anatomical_structure ,Cell culture ,Immunology ,Medicine ,Female ,Interleukin 17 ,Research Article - Abstract
Both interleukin (IL)-33 and IL-25 induce Th2 cytokine production by various cell types, suggesting that they contribute to development of allergic disorders. However, the precise roles of IL-33 and IL-25 in house dust mite (HDM)-induced allergic rhinitis (AR) remain unclear. Both IL-33 and IL-25 were produced mainly by nasal epithelial cells during HDM-induced AR. Eosinophil and goblet cell counts in the nose and IL-5 levels in lymph node cell culture supernatants were significantly decreased in IL-33-deficient, but not IL-25-deficient, mice compared with wild-type mice during HDM-induced AR, but the serum IgE and IgG1 levels did not differ. On the other hand, HDM-induced AR developed similarly in wild-type mice transferred with either IL-33-deficient BM cells or wild-type BM cells. IL-33, but not IL-25, produced by nasal epithelial cells was crucial for the development of murine HDM-induced AR. These observations suggest that IL-33 neutralization may be a potential approach for treatment of HDM-induced AR in humans.
- Published
- 2013