| First Author | Gibbert K | Year | 2012 |
| Journal | PLoS Pathog | Volume | 8 |
| Issue | 8 | Pages | e1002868 |
| PubMed ID | 22912583 | Mgi Jnum | J:222144 |
| Mgi Id | MGI:5644016 | Doi | 10.1371/journal.ppat.1002868 |
| Citation | Gibbert K, et al. (2012) Interferon-alpha subtype 11 activates NK cells and enables control of retroviral infection. PLoS Pathog 8(8):e1002868 |
| abstractText | The innate immune response mediated by cells such as natural killer (NK) cells is critical for the rapid containment of virus replication and spread during acute infection. Here, we show that subtype 11 of the type I interferon (IFN) family greatly potentiates the antiviral activity of NK cells during retroviral infection. Treatment of mice with IFN-alpha11 during Friend retrovirus infection (FV) significantly reduced viral loads and resulted in long-term protection from virus-induced leukemia. The effect of IFN-alpha11 on NK cells was direct and signaled through the type I IFN receptor. Furthermore, IFN-alpha11-mediated activation of NK cells enabled cytolytic killing of FV-infected target cells via the exocytosis pathway. Depletion and adoptive transfer experiments illustrated that NK cells played a major role in successful IFN-alpha11 therapy. Additional experiments with Mouse Cytomegalovirus infections demonstrated that the therapeutic effect of IFN-alpha11 is not restricted to retroviruses. The type I IFN subtypes 2 and 5, which bind the same receptor as IFN-alpha11, did not elicit similar antiviral effects. These results demonstrate a unique and subtype-specific activation of NK cells by IFN-alpha11. |
