| First Author | Nakanishi W | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 10 | Pages | e78099 |
| PubMed ID | 24205109 | Mgi Jnum | J:209237 |
| Mgi Id | MGI:5566740 | Doi | 10.1371/journal.pone.0078099 |
| Citation | Nakanishi W, et al. (2013) IL-33, but not IL-25, is crucial for the development of house dust mite antigen-induced allergic rhinitis. PLoS One 8(10):e78099 |
| abstractText | 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. |
