Stage-specific GATA3 induction promotes ILC2 development after lineage commitment

Hiroki Furuya, Yosuke Toda, Arifumi Iwata (), Mizuki Kanai, Kodai Kato, Takashi Kumagai, Takahiro Kageyama, Shigeru Tanaka, Lisa Fujimura, Akemi Sakamoto, Masahiko Hatano, Akira Suto, Kotaro Suzuki and Hiroshi Nakajima ()
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Hiroki Furuya: Chiba University
Yosuke Toda: Chiba University
Arifumi Iwata: Chiba University
Mizuki Kanai: Chiba University
Kodai Kato: Chiba University
Takashi Kumagai: Chiba University
Takahiro Kageyama: Chiba University
Shigeru Tanaka: Chiba University
Lisa Fujimura: Chiba University
Akemi Sakamoto: Chiba University
Masahiko Hatano: Chiba University
Akira Suto: Chiba University
Kotaro Suzuki: Chiba University
Hiroshi Nakajima: Chiba University

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Group 2 innate lymphoid cells (ILC2s) are a subset of innate lymphocytes that produce type 2 cytokines, including IL-4, IL-5, and IL-13. GATA3 is a critical transcription factor for ILC2 development at multiple stages. However, when and how GATA3 is induced to the levels required for ILC2 development remains unclear. Herein, we identify ILC2-specific GATA3-related tandem super-enhancers (G3SE) that induce high GATA3 in ILC2-committed precursors. G3SE-deficient mice exhibit ILC2 deficiency in the bone marrow, lung, liver, and small intestine with minimal impact on other ILC lineages or Th2 cells. Single-cell RNA-sequencing and subsequent flow cytometry analysis show that GATA3 induction mechanism, which is required for entering the ILC2 stage, is lost in IL-17RB+PD-1− late ILC2-committed precursor stage in G3SE-deficient mice. Cnot6l, part of the CCR4-NOT deadenylase complex, is a possible GATA3 target during ILC2 development. Our findings implicate a stage-specific regulatory mechanism for GATA3 expression during ILC2 development.

Date: 2024
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DOI: 10.1038/s41467-024-49881-y

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