Satb1 regulates the effector program of encephalitogenic tissue Th17 cells in chronic inflammation

被引:31
|
作者
Yasuda, Keiko [1 ,2 ,3 ]
Kitagawa, Yohko [2 ]
Kawakami, Ryoji [2 ]
Isaka, Yoshitaka [3 ]
Watanabe, Hitomi [4 ]
Kondoh, Gen [4 ]
Kohwi-Shigematsu, Terumi [5 ]
Sakaguchi, Shimon [1 ,2 ]
Hirota, Keiji [2 ,4 ]
机构
[1] Kyoto Univ, Expt Immunol Lab, Inst Frontier Life & Med Sci, Kyoto 6068507, Japan
[2] Osaka Univ, Immunol Frontier Res Ctr, Dept Expt Immunol, Osaka 5650871, Japan
[3] Osaka Univ, Dept Nephrol, Grad Sch Med, Osaka 5650871, Japan
[4] Kyoto Univ, Inst Frontier Life & Med Sci, Lab Integrat Biol Sci, Kyoto 6068507, Japan
[5] Univ Calif San Francisco, Dept Orofacial Sci, San Francisco, CA 94143 USA
关键词
PATHOGENIC T(H)17 CELLS; HELPER T-CELLS; TGF-BETA; GM-CSF; MONOCLONAL-ANTIBODY; DIFFERENTIATION; CYTOKINE; EXPRESSION; INDUCTION; RECEPTOR;
D O I
10.1038/s41467-019-08404-w
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The genome organizer, special AT-rich sequence-binding protein-1 (Satb1), plays a pivotal role in the regulation of global gene networks in a cell type-dependent manner and is indispensable for the development of multiple cell types, including mature CD4(+) T, CD8(+) T, and Foxp3(+) regulatory T cells in the thymus. However, it remains unknown how the differentiation and effector program of the Th subsets in the periphery are regulated by Satb1. Here, we demonstrate that Satb1 differentially regulates gene expression profiles in nonpathogenic and pathogenic Th17 cells and promotes the pathogenic effector program of encephalitogenic Th17 cells by regulating GM-CSF via Bhlhe40 and inhibiting PD-1 expression. However, Satb1 is dispensable for the differentiation and non-pathogenic functions of Th17 cells. These results indicate that Satb1 regulates the specific gene expression and function of effector Th17 cells in tissue inflammation.
引用
收藏
页数:14
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