Journal
EMBO MOLECULAR MEDICINE
Volume 6, Issue 1, Pages 120-140Publisher
WILEY
DOI: 10.1002/emmm.201302890
Keywords
IL-27; IL-17; gamma delta T cells; Streptococcus pneumoniae; influenza virus
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Funding
- National Natural Science Foundation of China [81370110, 81000711, 81200054, 81371778]
- Natural Science Foundation of Chongqing (CSTC) [2011BB5139]
- National Clinical Key Subject to the Department of Laboratory Medicine of the First Affiliated Hospital of Chongqing Medical University [20100305]
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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 gamma delta T cells but not alpha beta 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 gamma delta T cells activated by Streptococcus pneumoniae and dendritic cells. This suppressive activity of IL-27 on gamma delta T cells was dependent on transcription factor STAT1. Finally, neutralization of IL-27 or administration of IL-17A restored the role of gamma delta 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.
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