| First Author | Kunikata T | Year | 2005 |
| Journal | Nat Immunol | Volume | 6 |
| Issue | 5 | Pages | 524-31 |
| PubMed ID | 15806106 | Mgi Jnum | J:97735 |
| Mgi Id | MGI:3576187 | Doi | 10.1038/ni1188 |
| Citation | Kunikata T, et al. (2005) Suppression of allergic inflammation by the prostaglandin E receptor subtype EP3. Nat Immunol 6(5):524-31 |
| abstractText | Prostaglandins, including PGD(2) and PGE(2), are produced during allergic reactions. Although PGD(2) is an important mediator of allergic responses, aspirin-like drugs that inhibit prostaglandin synthesis are generally ineffective in allergic disorders, suggesting that another prostaglandin-mediated pathway prevents the development of allergic reactions. Here we show that such a pathway may be mediated by PGE(2) acting at the prostaglandin E receptor EP3. Mice lacking EP3 developed allergic inflammation that was much more pronounced than that in wild-type mice or mice deficient in other prostaglandin E receptor subtypes. Conversely, an EP3-selective agonist suppressed the inflammation. This suppression was effective when the agonist was administered 3 h after antigen challenge and was associated with inhibition of allergy-related gene expression. Thus, the PGE(2)-EP3 pathway is an important negative modulator of allergic reactions. |
