| First Author | Sandrock I | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 12 | Pages | 3006-3018 |
| PubMed ID | 30455268 | Mgi Jnum | J:269697 |
| Mgi Id | MGI:6272975 | Doi | 10.1084/jem.20181439 |
| Citation | Sandrock I, et al. (2018) Genetic models reveal origin, persistence and non-redundant functions of IL-17-producing gammadelta T cells. J Exp Med 215(12):3006-3018 |
| abstractText | gammadelta T cells are highly conserved in jawed vertebrates, suggesting an essential role in the immune system. However, gammadelta T cell-deficient Tcrd (-/-) mice display surprisingly mild phenotypes. We hypothesized that the lack of gammadelta T cells in constitutive Tcrd (-/-) mice is functionally compensated by other lymphocytes taking over genuine gammadelta T cell functions. To test this, we generated a knock-in model for diphtheria toxin-mediated conditional gammadelta T cell depletion. In contrast to IFN-gamma-producing gammadelta T cells, IL-17-producing gammadelta T cells (Tgammadelta17 cells) recovered inefficiently after depletion, and their niches were filled by expanding Th17 cells and ILC3s. Complementary genetic fate mapping further demonstrated that Tgammadelta17 cells are long-lived and persisting lymphocytes. Investigating the function of gammadelta T cells, conditional depletion but not constitutive deficiency protected from imiquimod-induced psoriasis. Together, we clarify that fetal thymus-derived Tgammadelta17 cells are nonredundant local effector cells in IL-17-driven skin pathology. |
