| First Author | Moriwaki A | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 404 |
| Issue | 4 | Pages | 922-7 |
| PubMed ID | 21184733 | Mgi Jnum | J:168469 |
| Mgi Id | MGI:4888426 | Doi | 10.1016/j.bbrc.2010.12.082 |
| Citation | Moriwaki A, et al. (2011) IL-13 suppresses double-stranded RNA-induced IFN-lambda production in lung cells. Biochem Biophys Res Commun 404(4):922-7 |
| abstractText | Acute asthma exacerbations are frequently associated with respiratory viral infections. Although impaired production of type III IFNs (IFN-lambdas) is related to the severity of asthma exacerbation, the mechanisms underlying deficient IFN-lambda production in asthma are poorly understood. Airway epithelial cells were stimulated in vitro with a synthetic mimetic of viral double-stranded RNA (dsRNA). IL-13, a crucial cytokine responsible for asthma pathogenesis, suppressed dsRNA-induced expression of IFN-lambdas, and JAK inhibitor AG490 prevented the suppression by IL-13. IL-13 per se did not affect IFN-lambda production or the expressions of membrane dsRNA receptor TLR3 and of cytoplasmic receptors RIG-I and MDA5. IL-13-deficient mice exhibited more enhanced IFN-lambda expression after intratracheal instillation of dsRNA than wild-type mice, whereas IFN-lambda expression after dsRNA was absent in the mouse lungs of the OVA-induced asthma model. These findings suggest that IL-13 may be a putative cytokine suppressing IFN-lambda production against airway viral infections in asthmatics. |
