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

Keiko Yasuda, Yohko Kitagawa, Ryoji Kawakami, Yoshitaka Isaka, Hitomi Watanabe, Gen Kondoh, Terumi Kohwi-Shigematsu, Shimon Sakaguchi () and Keiji Hirota ()
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Keiko Yasuda: Kyoto University
Yohko Kitagawa: Osaka University
Ryoji Kawakami: Osaka University
Yoshitaka Isaka: Osaka University Graduate School of Medicine
Hitomi Watanabe: Kyoto University
Gen Kondoh: Kyoto University
Terumi Kohwi-Shigematsu: University of California
Shimon Sakaguchi: Kyoto University
Keiji Hirota: Osaka University

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract 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 non-pathogenic 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.

Date: 2019
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DOI: 10.1038/s41467-019-08404-w

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