| First Author | Kinyanjui MW | Year | 2013 |
| Journal | J Immunol | Volume | 190 |
| Issue | 8 | Pages | 3859-68 |
| PubMed ID | 23509346 | Mgi Jnum | J:195113 |
| Mgi Id | MGI:5476551 | Doi | 10.4049/jimmunol.1200506 |
| Citation | Kinyanjui MW, et al. (2013) Dose-Dependent Effects of IL-17 on IL-13-Induced Airway Inflammatory Responses and Airway Hyperresponsiveness. J Immunol 190(8):3859-68 |
| abstractText | The Th2 cytokine IL-13 regulates several aspects of the asthmatic phenotype, including airway inflammation, airway hyperresponsiveness, and mucus production. The Th17 cytokine IL-17A is also implicated in asthma and has been shown to both positively and negatively regulate Th2-dependent responses in murine models of allergic airways disease. Our objective in this study was to better understand the role of IL-17 in airway inflammation by examining how IL-17 modifies IL-13-induced airway inflammatory responses. We treated BALB/c mice intranasally with IL-13 or IL-17 alone or in combination for 8 consecutive days, after which airway hyperresponsiveness, inflammatory cell influx into the lung, and lung chemokine/cytokine expression were assessed. As expected, IL-13 increased airway inflammation and airway hyperresponsiveness. IL-13 also increased numbers of IL-17-producing CD4(+) and gammadelta T cells. Treating mice with a combination of IL-13 and IL-17 reduced infiltration of IL-17(+) gammadelta T cells, but increased the number of infiltrating eosinophils. In contrast, coadministration of IL-13 with a higher dose of IL-17 decreased all IL-13-induced inflammatory responses, including infiltration of both IL-17(+)CD4(+) and gammadelta T cells. To examine the inhibitory activity of IL-17-expressing gammadelta T cells in this model, these cells were adoptively transferred into naive recipients. Consistent with an inhibitory role for gammadelta T cells, IL-13-induced infiltration of eosinophils, lymphocytes, and IL-17(+)CD4(+) T cells was diminished in recipients of the gammadelta T cells. Collectively, our data indicate that allergic airway inflammatory responses induced by IL-13 are modulated by both the quantity and the cellular source of IL-17. |
