PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

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.
PMID
Related Publications

Lymphotoxin-β receptor-independent development of intestinal IL-22-producing NKp46+ innate lymphoid cells.

Gata3 drives development of RORγt+ group 3 innate lymphoid cells.

TCF-1 controls ILC2 and NKp46+RORγt+ innate lymphocyte differentiation and protection in intestinal inflammation.

Group 3 innate lymphoid cells continuously require the transcription factor GATA-3 after commitment.

Transcription Factor Bcl11b Controls Identity and Function of Mature Type 2 Innate Lymphoid Cells.

Authors

Mayor MeshTerms

Immunity, Innate

Keywords
Journal Title nature immunology
Publication Year Start




PMID- 26414766
OWN - NLM
STAT- MEDLINE
DA  - 20151020
DCOM- 20160422
LR  - 20170902
IS  - 1529-2916 (Electronic)
IS  - 1529-2908 (Linking)
VI  - 16
IP  - 11
DP  - 2015 Nov
TI  - Runx3 specifies lineage commitment of innate lymphoid cells.
PG  - 1124-33
LID - 10.1038/ni.3272 [doi]
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 RORgammat
      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.
FAU - Ebihara, Takashi
AU  - Ebihara T
AUID- ORCID: http://orcid.org/0000-0001-7489-1051
AD  - Howard Hughes Medical Institute, Washington University School of Medicine, St.
      Louis, Missouri, USA.
FAU - Song, Christina
AU  - Song C
AD  - Department of Pathology and Immunology, Washington University School of Medicine,
      St. Louis, Missouri, USA.
FAU - Ryu, Stacy H
AU  - Ryu SH
AUID- ORCID: http://orcid.org/0000-0002-5448-339X
AD  - Department of Pathology and Immunology, Washington University School of Medicine,
      St. Louis, Missouri, USA.
FAU - Plougastel-Douglas, Beatrice
AU  - Plougastel-Douglas B
AD  - Division of Rheumatology, Department of Medicine, Washington University School of
      Medicine, St. Louis, Missouri, USA.
FAU - Yang, Liping
AU  - Yang L
AD  - Division of Rheumatology, Department of Medicine, Washington University School of
      Medicine, St. Louis, Missouri, USA.
FAU - Levanon, Ditsa
AU  - Levanon D
AD  - Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot,
      Israel.
FAU - Groner, Yoram
AU  - Groner Y
AD  - Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot,
      Israel.
FAU - Bern, Michael D
AU  - Bern MD
AD  - Division of Rheumatology, Department of Medicine, Washington University School of
      Medicine, St. Louis, Missouri, USA.
AD  - Medical Scientist Training Program, Washington University School of Medicine, St.
      Louis, Missouri, USA.
FAU - Stappenbeck, Thaddeus S
AU  - Stappenbeck TS
AD  - Department of Pathology and Immunology, Washington University School of Medicine,
      St. Louis, Missouri, USA.
FAU - Colonna, Marco
AU  - Colonna M
AD  - Department of Pathology and Immunology, Washington University School of Medicine,
      St. Louis, Missouri, USA.
FAU - Egawa, Takeshi
AU  - Egawa T
AD  - Department of Pathology and Immunology, Washington University School of Medicine,
      St. Louis, Missouri, USA.
FAU - Yokoyama, Wayne M
AU  - Yokoyama WM
AD  - Howard Hughes Medical Institute, Washington University School of Medicine, St.
      Louis, Missouri, USA.
AD  - Division of Rheumatology, Department of Medicine, Washington University School of
      Medicine, St. Louis, Missouri, USA.
LA  - eng
GR  - HHMI_YOKOYAMA_W/Howard Hughes Medical Institute/United States
GR  - R01 DK071619/DK/NIDDK NIH HHS/United States
GR  - R01AI097244/AI/NIAID NIH HHS/United States
GR  - R01 AI097244/AI/NIAID NIH HHS/United States
GR  - T32 GM007200/GM/NIGMS NIH HHS/United States
GR  - T32-GM007200/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20150928
PL  - United States
TA  - Nat Immunol
JT  - Nature immunology
JID - 100941354
RN  - 0 (Ahr protein, mouse)
RN  - 0 (Antigens, Ly)
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (Cbfb protein, mouse)
RN  - 0 (Core Binding Factor Alpha 3 Subunit)
RN  - 0 (Core Binding Factor beta Subunit)
RN  - 0 (Interleukin-7 Receptor alpha Subunit)
RN  - 0 (Natural Cytotoxicity Triggering Receptor 1)
RN  - 0 (Ncr1 protein, mouse)
RN  - 0 (Nuclear Receptor Subfamily 1, Group F, Member 3)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 0 (Rorc protein, mouse)
RN  - 0 (Runx3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Antigens, Ly/metabolism
MH  - Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism
MH  - Cell Differentiation/immunology
MH  - Cell Lineage/immunology
MH  - Citrobacter rodentium/immunology/pathogenicity
MH  - Core Binding Factor Alpha 3 Subunit/deficiency/genetics/*metabolism
MH  - Core Binding Factor beta Subunit/deficiency/genetics/metabolism
MH  - Enterobacteriaceae Infections/etiology/immunology
MH  - *Immunity, Innate
MH  - Interleukin-7 Receptor alpha Subunit/metabolism
MH  - Intestinal Mucosa/cytology/immunology
MH  - Lymphocyte Subsets/cytology/*immunology/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Natural Cytotoxicity Triggering Receptor 1/metabolism
MH  - Nuclear Receptor Subfamily 1, Group F, Member 3/deficiency/genetics/metabolism
MH  - Receptors, Aryl Hydrocarbon/genetics/metabolism
PMC - PMC4618046
MID - NIHMS714852
OID - NLM: NIHMS714852
OID - NLM: PMC4618046
EDAT- 2015/09/29 06:00
MHDA- 2016/04/23 06:00
CRDT- 2015/09/29 06:00
PHST- 2015/05/21 [received]
PHST- 2015/08/10 [accepted]
AID - ni.3272 [pii]
AID - 10.1038/ni.3272 [doi]
PST - ppublish
SO  - Nat Immunol. 2015 Nov;16(11):1124-33. doi: 10.1038/ni.3272. Epub 2015 Sep 28.