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PLoS One. 2016 Jun 10;11(6):e0157395. doi: 10.1371/journal.pone.0157395. eCollection 2016.

The Transcriptional Repressor Gfi1 Plays a Critical Role in the Development of NKT1- and NKT2-Type iNKT Cells.

Author information

1
Department of Obstetrics and Gynecology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
2
Department of Immunology, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
3
Translational Research Center, Ehime University Hospital, Shitsukawa, Toon, Ehime, Japan.
4
Division of Immune Regulation, Department of Proteo-Inovation, Proteo-Science Center, Ehime University, Toon, Ehime, Japan.
5
Department of Infection and Host Defenses, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
6
Department of Hematology, Clinical Immunology and Infectious Diseases, Graduate School of Medicine, Ehime University, Shitsukawa, Toon, Ehime, Japan.
7
Laboratory of Immune Regulation, RIKEN Center for Integrative Medical Sciences, 1-7-22 suehiro-cho, Tsurumi-ku, Yokohama, Japan.

Abstract

Gfi1 plays an important role in the development and maintenance of many hematopoietic linage cells. However, the impact of Gfi1-deficiency on the iNKT cell differentiation remains unclear. We herein demonstrate a critical role of Gfi1 in regulating the development of iNKT cell subsets. In the thymus of T cell-specific Gfi1-deficient mice, iNKT cells normally developed up to stage 2, while the number of stage 3 NK1.1pos iNKT cells was significantly reduced. Furthermore, CD4pos iNKT cells were selectively reduced in the peripheral organs of T cell-specific Gfi1-deficient mice. The α-GalCer-dependent production of IFN-γand Th2 cytokines, but not IL-17A, was severely reduced in T cell-specific Gfi1-deficient mice. In addition, a reduction of the α-GalCer-induced anti-tumor activity was observed in Gfi1-deficient mice. These findings demonstrate the important role of Gfi1 in regulating the development and function of NKT1- and NKT2-type iNKT cell subsets.

PMID:
27284976
PMCID:
PMC4902269
DOI:
10.1371/journal.pone.0157395
[Indexed for MEDLINE]
Free PMC Article

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