Nfil3 is required for the development of all innate lymphoid cell subsets

Seillet, Cyril; Rankin, Lucille C.; Groom, Joanna R; Mielke, Lisa A.; Tellier, Julie; Chopin, Michaël; Huntington, Nicholas D.; Belz, Gabrielle T.; Carotta, Sebastian

doi:10.1084/jem.20140145

Cited by 212 publications

(175 citation statements)

References 21 publications

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“…[42][43][44] Nfil3-deficient mice display a severe defect in NK-cell development, 45,46 in addition to impaired development of CD8 1 and CD103 1 conventional DC subsets, B cells, and other innate lymphoid subsets. 44,[47][48][49] Reduced GATA-2-mediated induction of NFIL-3 could thus contribute to DC, B-cell, and NK-cell cytopenias observed in humans with GATA-2 haploinsufficiency, as suggested by our findings of reduced NK-cell output from Lin 2 cell progenitors in patients with GATA2 mutation. Interestingly, CMV infection bypasses the requirement for Nfil3 in mouse NK-cell development, supporting generation of long-lived, adaptive NK cells.…”

Section: Discussionmentioning

confidence: 56%

Adaptive NK cells can persist in patients with GATA2 mutation depleted of stem and progenitor cells

Schlums

Jung

Han

et al. 2017

Blood

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Section: Discussionmentioning

confidence: 56%

Adaptive NK cells can persist in patients with GATA2 mutation depleted of stem and progenitor cells

Schlums

Jung

Han

et al. 2017

Blood

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“…The second group consists of genes that are normally not activated to substantial levels at all during the phase 1 stages. Curiously, these are highly enriched for genes used in NK cells, ILCs, and innate-like T cells, including the powerful regulatory genes Id2, Zbtb16, and Nfil3 (6,42,(49)(50)(51)(52)(53)(54)(55). Many of these genes, especially NK-associated genes, require continual Bcl11b action to keep them silent later (Fig.…”

Section: Discussionmentioning

confidence: 99%

Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network

Longabaugh

Zeng

Zhang

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

148

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T-cell development from hematopoietic progenitors depends on multiple transcription factors, mobilized and modulated by intrathymic Notch signaling. Key aspects of T-cell specification network architecture have been illuminated through recent reports defining roles of transcription factors PU.1, GATA-3, and E2A, their interactions with Notch signaling, and roles of Runx1, TCF-1, and Hes1, providing bases for a comprehensively updated model of the T-cell specification gene regulatory network presented herein. However, the role of lineage commitment factor Bcl11b has been unclear. We use self-organizing maps on 63 RNA-seq datasets from normal and perturbed T-cell development to identify functional targets of Bcl11b during commitment and relate them to other regulomes. We show that both activation and repression target genes can be bound by Bcl11b in vivo, and that Bcl11b effects overlap with E2A-dependent effects. The newly clarified role of Bcl11b distinguishes discrete components of commitment, resolving how innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mechanisms.

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“…1). Progressive commitment to the ILC lineage is also dependent, to varying degrees, on a multitude of transcription factors including GATA‐3, TOX, TCF‐1 and NFIL316, 17, 18, 19, 20, 21 (and reviewed in detail in references 10 and 22). …”

Section: Group 3 Innate Lymphoid Cell Developmentmentioning

confidence: 99%

Functional and phenotypic heterogeneity of group 3 innate lymphoid cells

2017

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SummaryGroup 3 innate lymphoid cells (ILC3), defined by expression of the transcription factor retinoid‐related orphan receptor γt, play key roles in the regulation of inflammation and immunity in the gastrointestinal tract and associated lymphoid tissues. ILC3 consist largely of two major subsets, NCR + ILC3 and LTi‐like ILC3, but also demonstrate significant plasticity and heterogeneity. Recent advances have begun to dissect the relationship between ILC3 subsets and to define distinct functional states within the intestinal tissue microenvironment. In this review we discuss the ever‐expanding roles of ILC3 in the context of intestinal homeostasis, infection and inflammation – with a focus on comparing and contrasting the relative contributions of ILC3 subsets.

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Nfil3 is required for the development of all innate lymphoid cell subsets

Abstract: Loss of Nfil3 selectively reduces Peyer’s patch formation, impairing recruitment and distribution of lymphocytes and compromising immune responses to inflammatory and infectious agents.

Cited by 212 publications

References 21 publications

Adaptive NK cells can persist in patients with GATA2 mutation depleted of stem and progenitor cells

Adaptive NK cells can persist in patients with GATA2 mutation depleted of stem and progenitor cells

Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network

Functional and phenotypic heterogeneity of group 3 innate lymphoid cells

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