| First Author | Hernández PP | Year | 2015 |
| Journal | Nat Immunol | Volume | 16 |
| Issue | 7 | Pages | 698-707 |
| PubMed ID | 26006013 | Mgi Jnum | J:260611 |
| Mgi Id | MGI:6142537 | Doi | 10.1038/ni.3180 |
| Citation | Hernandez PP, et al. (2015) Interferon-lambda and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection. Nat Immunol 16(7):698-707 |
| abstractText | The epithelium is the main entry point for many viruses, but the processes that protect barrier surfaces against viral infections are incompletely understood. Here we identified interleukin 22 (IL-22) produced by innate lymphoid cell group 3 (ILC3) as an amplifier of signaling via interferon-lambda (IFN-lambda), a synergism needed to curtail the replication of rotavirus, the leading cause of childhood gastroenteritis. Cooperation between the receptor for IL-22 and the receptor for IFN-lambda, both of which were ''preferentially'' expressed by intestinal epithelial cells (IECs), was required for optimal activation of the transcription factor STAT1 and expression of interferon-stimulated genes (ISGs). These data suggested that epithelial cells are protected against viral replication by co-option of two evolutionarily related cytokine networks. These data may inform the design of novel immunotherapy for viral infections that are sensitive to interferons. |
