4.6 Article

IL-33, but Not IL-25, Is Crucial for the Development of House Dust Mite Antigen-Induced Allergic Rhinitis

Journal

PLOS ONE
Volume 8, Issue 10, Pages -

Publisher

PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0078099

Keywords

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Funding

  1. Global COE Program
  2. Ministry of Education, Culture, Sports, Science and Technology (MEXT)
  3. Ministry of Health, Labour and Welfare, Japan
  4. Grant of National Center for Child Health and Development [23A-5]
  5. Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency
  6. Grants-in-Aid for Scientific Research [25860805, 25461168, 23390262] Funding Source: KAKEN

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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.

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