Runx3 specifies lineage commitment of innate lymphoid cells

Takashi Ebihara; Christina Song; Stacy H. Ryu; Beatrice Plougastel-Douglas; Liping Yang; Ditsa Levanon; Yoram Groner; Michael D. Bern; Thaddeus S. Stappenbeck; Marco Colonna; Takeshi Egawa; Wayne M. Yokoyama

doi:10.1038/ni.3272

Runx3 specifies lineage commitment of innate lymphoid cells

Takashi Ebihara, Christina Song, Stacy H. Ryu, Beatrice Plougastel-Douglas, Liping Yang, Ditsa Levanon, Yoram Groner, Michael D. Bern, Thaddeus S. Stappenbeck, Marco Colonna, Takeshi Egawa, Wayne M. Yokoyama

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145 Scopus citations

Abstract

Subsets of innate lymphoid cells (ILCs) reside in the mucosa and regulate immune responses to external pathogens. While ILCs can be phenotypically classified into ILC1, ILC2 and ILC3 subsets, the transcriptional control of commitment to each ILC lineage is incompletely understood. Here we report that the transcription factor Runx3 was essential for the normal development of ILC1 and ILC3 cells but not of ILC2 cells. Runx3 controlled the survival of ILC1 cells but not of ILC3 cells. Runx3 was required for expression of the transcription factor RORγt and its downstream target, the transcription factor AHR, in ILC3 cells. The absence of Runx3 in ILCs exacerbated infection with Citrobacter rodentium. Therefore, our data establish Runx3 as a key transcription factor in the lineage-specific differentiation of ILC1 and ILC3 cells.

Original language	English
Pages (from-to)	1124-1133
Number of pages	10
Journal	Nature immunology
Volume	16
Issue number	11
DOIs	https://doi.org/10.1038/ni.3272
State	Published - Oct 20 2015

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title = "Runx3 specifies lineage commitment of innate lymphoid cells",

abstract = "Subsets of innate lymphoid cells (ILCs) reside in the mucosa and regulate immune responses to external pathogens. While ILCs can be phenotypically classified into ILC1, ILC2 and ILC3 subsets, the transcriptional control of commitment to each ILC lineage is incompletely understood. Here we report that the transcription factor Runx3 was essential for the normal development of ILC1 and ILC3 cells but not of ILC2 cells. Runx3 controlled the survival of ILC1 cells but not of ILC3 cells. Runx3 was required for expression of the transcription factor RORγt and its downstream target, the transcription factor AHR, in ILC3 cells. The absence of Runx3 in ILCs exacerbated infection with Citrobacter rodentium. Therefore, our data establish Runx3 as a key transcription factor in the lineage-specific differentiation of ILC1 and ILC3 cells.",

author = "Takashi Ebihara and Christina Song and Ryu, {Stacy H.} and Beatrice Plougastel-Douglas and Liping Yang and Ditsa Levanon and Yoram Groner and Bern, {Michael D.} and Stappenbeck, {Thaddeus S.} and Marco Colonna and Takeshi Egawa and Yokoyama, {Wayne M.}",

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AU - Song, Christina

AU - Ryu, Stacy H.

AU - Plougastel-Douglas, Beatrice

AU - Yang, Liping

AU - Levanon, Ditsa

AU - Groner, Yoram

AU - Bern, Michael D.

AU - Stappenbeck, Thaddeus S.

AU - Colonna, Marco

AU - Egawa, Takeshi

AU - Yokoyama, Wayne M.

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AB - Subsets of innate lymphoid cells (ILCs) reside in the mucosa and regulate immune responses to external pathogens. While ILCs can be phenotypically classified into ILC1, ILC2 and ILC3 subsets, the transcriptional control of commitment to each ILC lineage is incompletely understood. Here we report that the transcription factor Runx3 was essential for the normal development of ILC1 and ILC3 cells but not of ILC2 cells. Runx3 controlled the survival of ILC1 cells but not of ILC3 cells. Runx3 was required for expression of the transcription factor RORγt and its downstream target, the transcription factor AHR, in ILC3 cells. The absence of Runx3 in ILCs exacerbated infection with Citrobacter rodentium. Therefore, our data establish Runx3 as a key transcription factor in the lineage-specific differentiation of ILC1 and ILC3 cells.

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Runx3 specifies lineage commitment of innate lymphoid cells

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