| First Author | Lu Y | Year | 2015 |
| Journal | J Immunol | Volume | 195 |
| Issue | 9 | Pages | 4273-81 |
| PubMed ID | 26408661 | Mgi Jnum | J:262271 |
| Mgi Id | MGI:6158237 | Doi | 10.4049/jimmunol.1500939 |
| Citation | Lu Y, et al. (2015) PLZF Controls the Development of Fetal-Derived IL-17+Vgamma6+ gammadelta T Cells. J Immunol 195(9):4273-81 |
| abstractText | Expression of promyelocytic leukemia zinc finger (PLZF) protein directs the effector differentiation of invariant NKT (iNKT) cells and IL-4(+) gammadelta NKT cells. In this study, we show that PLZF is also required for the development and function of IL-17(+) gammadelta T cells. We observed that PLZF is expressed in fetal-derived invariant Vgamma5(+) and Vgamma6(+) gammadelta T cells, which secrete IFN-gamma and IL-17, respectively. PLZF deficiency specifically affected the effector differentiation of Vgamma6(+) cells, leading to reduced numbers of mature CD27(-)CD44(+) phenotype capable of secreting IL-17. Although PLZF was not required for Vgamma5(+) gammadelta T cells to develop, when these cells were reprogrammed into IL-17-secreting cells in Skint-1 mutant mice, they required PLZF for their effector maturation, similarly to Vgamma6(+) gammadelta T cells. The impaired effector differentiation of PLZF-deficient Vgamma6(+) gammadelta T cells was not due to increased apoptosis and it was related to reduced proliferation of immature CD27(+)CD44(-) Vgamma6(+) gammadelta T cells, which was required for their differentiation into mature CD27(-)CD44(+) IL-17-secreting cells. Thus, the present study identifies that PLZF function is not restricted to NKT or IL-4(+) T cells, but it also controls the development of IL-17(+) gammadelta T cells. |
