Format

Send to

Choose Destination
Front Immunol. 2018 Feb 28;9:196. doi: 10.3389/fimmu.2018.00196. eCollection 2018.

Transcription Factor KLF10 Constrains IL-17-Committed Vγ4+ γδ T Cells.

Author information

1
Department of Agricultural Biotechnology and Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, South Korea.
2
Academy of Immunology and Microbiology, Institute for Basic Science, Pohang, South Korea.
3
College of Medicine, Inha University, Incheon, South Korea.
4
Department of Animal Biotechnology, Chonbuk National University, Jeonju, South Korea.
5
Division of Bacterial Disease Research, Center for Infectious Disease Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong, South Korea.
6
Department of Immunology, Laboratory of Dendritic Cell Differentiation and Regulation, School of Medicine, Konkuk University, Chungju, South Korea.
7
Department of Oral Microbiology and Immunology, DRI and BK21 Plus Program, School of Dentistry, Seoul National University, Seoul, South Korea.
8
Center for Food Bioconvergence, Seoul National University, Seoul, South Korea.
9
Institute of Green Bio Science Technology, Seoul National University, Pyeongchang, South Korea.

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.

KEYWORDS:

IL-17; Innate-like γδ-17; KLF10; homeostasis; γδ T cells

PMID:
29541070
PMCID:
PMC5835516
DOI:
10.3389/fimmu.2018.00196
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Frontiers Media SA Icon for PubMed Central
Loading ...
Support Center