AUTHOR=Kim Girak , Gu Min Jeong , Kim Soo Ji , Ko Kwang Hyun , Kye Yoon-Chul , Kim Cheol Gyun , Cho Jae-Ho , Lee Woon-Kyu , Song Ki-Duk , Chu Hyuk , Park Yeong-Min , Han Seung Hyun , Yun Cheol-Heui TITLE=Transcription Factor KLF10 Constrains IL-17-Committed Vγ4+ γδ T Cells JOURNAL=Frontiers in Immunology VOLUME=9 YEAR=2018 URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2018.00196 DOI=10.3389/fimmu.2018.00196 ISSN=1664-3224 ABSTRACT=

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− γδ T (γδ27−-17) cells. We found selective augmentation of Vγ4+ γδ27− cells with higher IL-17 production in KLF10-deficient mice. Surprisingly, KLF10-deficient CD127hi Vγ4+ γδ27−-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+ γδ27− 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+ γδ27−-17 cells. Collectively, these findings demonstrate that KLF10 regulates thymic development of Vγ4+ γδ27− cells and their peripheral homeostasis at steady state.