| First Author | Chen Y | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 3 | Pages | 1163-1169 |
| PubMed ID | 28637904 | Mgi Jnum | J:250895 |
| Mgi Id | MGI:6100195 | Doi | 10.4049/jimmunol.1602144 |
| Citation | Chen Y, et al. (2017) IFN-gamma-Expressing Th17 Cells Are Required for Development of Severe Ocular Surface Autoimmunity. J Immunol 199(3):1163-1169 |
| abstractText | Th17 cells are critical effectors mediating the ocular surface autoimmunity in dry eye disease (DED). Increased IFN-gamma has also been implicated in DED; however, it remains unclear to what extent Th1 cells contribute to DED pathogenesis. In this study, we investigated the cellular source of IFN-gamma and assessed its contribution to corneal epitheliopathy in DED mice. We discovered a significant IL-17A(+)IFN-gamma(+) (Th17/1) population and determined that these cells are derived from Th17 precursors. Adoptive transfer of Th17/1, but not Th1, cells confers the disease to naive recipients as effectively as do Th17 cells alone. DED-induced IL-12 and IL-23 are required for in vivo transition of pathogenic Th17 cells to IFN-gamma producers. Furthermore, using IFN-gamma-deficient Th17 cells, we demonstrate the disease-amplifying role of Th17-derived IFN-gamma in DED pathogenesis. These results clearly demonstrate that Th17 cells mediate ocular surface autoimmunity through both IL-17A and IFN-gamma. |
