| First Author | Cao J | Year | 2014 |
| Journal | EMBO Mol Med | Volume | 6 |
| Issue | 1 | Pages | 120-40 |
| PubMed ID | 24408967 | Mgi Jnum | J:232300 |
| Mgi Id | MGI:5776457 | Doi | 10.1002/emmm.201302890 |
| Citation | Cao J, et al. (2014) Activation of IL-27 signalling promotes development of postinfluenza pneumococcal pneumonia. EMBO Mol Med 6(1):120-40 |
| abstractText | Postinfluenza pneumococcal pneumonia is a common cause of death in humans. However, the role of IL-27 in the pathogenesis of secondary pneumococcal pneumonia after influenza is unknown. We now report that influenza infection induced pulmonary IL-27 production in a type I IFN-alpha/beta receptor (IFNAR) signalling-dependent manner, which sensitized mice to secondary pneumococcal infection downstream of IFNAR pathway. Mice deficient in IL-27 receptor were resistant to secondary pneumococcal infection and generated more IL-17A-producing gammadelta T cells but not alphabeta T cells, thereby leading to enhanced neutrophil response during the early phase of host defence. IL-27 treatment could suppress the development of IL-17A-producing gammadelta T cells activated by Streptococcus pneumoniae and dendritic cells. This suppressive activity of IL-27 on gammadelta T cells was dependent on transcription factor STAT1. Finally, neutralization of IL-27 or administration of IL-17A restored the role of gammadelta T cells in combating secondary pneumococcal infection. Our study defines what we believe to be a novel role of IL-27 in impairing host innate immunity against pneumococcal infection. |
