<p>γδ 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 γδ 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<sup>−</sup> γδ T (γδ<sup>27−</sup>-17) cells. We found selective augmentation of Vγ4<sup>+</sup> γδ<sup>27−</sup> cells with higher IL-17 production in KLF10-deficient mice. Surprisingly, KLF10-deficient CD127<sup>hi</sup> Vγ4<sup>+</sup> γδ<sup>27−</sup>-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 Vγ4<sup>+</sup> γδ<sup>27−</sup> 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 Vγ4<sup>+</sup> γδ<sup>27−</sup>-17 cells. Collectively, these findings demonstrate that KLF10 regulates thymic development of Vγ4<sup>+</sup> γδ<sup>27−</sup> cells and their peripheral homeostasis at steady state.</p