Cutting Edge: Eomesodermin Is Sufficient To Direct Type 1 Innate Lymphocyte Development into the Conventional NK Lineage

Type 1 innate lymphocytes comprise two developmentally divergent lineages, type 1 helper innate lymphoid cells (hILC1s) and conventional NK cells (cNKs). All type 1 innate lymphocytes (ILCs) express the transcription factor T-bet, but cNKs additionally express Eomesodermin (Eomes). We show that dele...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2016-02, Vol.196 (4), p.1449-1454
Main Authors: Pikovskaya, Olga, Chaix, Julie, Rothman, Nyanza J, Collins, Amélie, Chen, Yen-Hua, Scipioni, Anna M, Vivier, Eric, Reiner, Steven L
Format: Article
Language:English
Subjects:
Animals
CD4-Positive T-Lymphocytes - immunology
Cell Differentiation
Cell Lineage
Core Binding Factor Alpha 3 Subunit - genetics
Core Binding Factor Alpha 3 Subunit - metabolism
Immunology
Killer Cells, Natural - immunology
Life Sciences
Mice, Transgenic
T-Box Domain Proteins - genetics
T-Box Domain Proteins - metabolism
Th1 Cells - immunology
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Summary:Type 1 innate lymphocytes comprise two developmentally divergent lineages, type 1 helper innate lymphoid cells (hILC1s) and conventional NK cells (cNKs). All type 1 innate lymphocytes (ILCs) express the transcription factor T-bet, but cNKs additionally express Eomesodermin (Eomes). We show that deletion of Eomes alleles at the onset of type 1 ILC maturation using NKp46-Cre imposes a substantial block in cNK development. Formation of the entire lymphoid and nonlymphoid type 1 ILC compartment appears to require the semiredundant action of both T-bet and Eomes. To determine if Eomes is sufficient to redirect hILC1 development to a cNK fate, we generated transgenic mice that express Eomes when and where T-bet is expressed using Tbx21 locus control to drive expression of Eomes codons. Ectopic Eomes induces cNK-like properties across the lymphoid and nonlymphoid type 1 ILC compartments. Subsequent to their divergent lineage specification, hILC1s and cNKs thus possess substantial developmental plasticity.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1502396