| First Author | Kim G | Year | 2018 |
| Journal | Front Immunol | Volume | 9 |
| Pages | 196 | PubMed ID | 29541070 |
| Mgi Jnum | J:313984 | Mgi Id | MGI:6791670 |
| Doi | 10.3389/fimmu.2018.00196 | Citation | Kim G, et al. (2018) Transcription Factor KLF10 Constrains IL-17-Committed Vgamma4(+) gammadelta T Cells. Front Immunol 9:196 |
| abstractText | gammadelta T cells, known to be an important source of innate IL-17 in mice, provide critical contributions to host immune responses. Development and function of gammadelta T cells are directed by networks of diverse transcription factors (TFs). Here, we examine the role of the zinc finger TFs, Kruppel-like factor 10 (KLF10), in the regulation of IL-17-committed CD27(-) gammadelta T (gammadelta(27-)-17) cells. We found selective augmentation of Vgamma4(+) gammadelta(27-) cells with higher IL-17 production in KLF10-deficient mice. Surprisingly, KLF10-deficient CD127(hi) Vgamma4(+) gammadelta(27-)-17 cells expressed higher levels of CD5 than their wild-type counterparts, with hyper-responsiveness to cytokine, but not T-cell receptor, stimuli. Thymic maturation of Vgamma4(+) gammadelta(27-) cells was enhanced in newborn mice deficient in KLF10. Finally, a mixed bone marrow chimera study indicates that intrinsic KLF10 signaling is requisite to limit Vgamma4(+) gammadelta(27-)-17 cells. Collectively, these findings demonstrate that KLF10 regulates thymic development of Vgamma4(+) gammadelta(27-) cells and their peripheral homeostasis at steady state. |
