| First Author | Taylor PR | Year | 2014 |
| Journal | Nat Immunol | Volume | 15 |
| Issue | 2 | Pages | 143-51 |
| PubMed ID | 24362892 | Mgi Jnum | J:209279 |
| Mgi Id | MGI:5566917 | Doi | 10.1038/ni.2797 |
| Citation | Taylor PR, et al. (2014) Activation of neutrophils by autocrine IL-17A-IL-17RC interactions during fungal infection is regulated by IL-6, IL-23, RORgammat and dectin-2. Nat Immunol 15(2):143-51 |
| abstractText | Here we identified a population of bone marrow neutrophils that constitutively expressed the transcription factor RORgammat and produced and responded to interleukin 17A (IL-17A (IL-17)). IL-6, IL-23 and RORgammat, but not T cells or natural killer (NK) cells, were required for IL-17 production in neutrophils. IL-6 and IL-23 induced expression of the receptors IL-17RC and dectin-2 on neutrophils, and IL-17RC expression was augmented by activation of dectin-2. Autocrine activity of IL-17A and its receptor induced the production of reactive oxygen species (ROS), and increased fungal killing in vitro and in a model of Aspergillus-induced keratitis. Human neutrophils also expressed RORgammat and induced the expression of IL-17A, IL-17RC and dectin-2 following stimulation with IL-6 and IL-23. Our findings identify a population of human and mouse neutrophils with autocrine IL-17 activity that probably contribute to the etiology of microbial and inflammatory diseases. |
