期刊
JOURNAL OF IMMUNOLOGY
卷 196, 期 4, 页码 1449-1454出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1502396
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资金
- National Institutes of Health [R01 AI061699, R01 AI113365, F30 AI113963]
- European Research Council THINK Advanced Grant
- Equipe Labellisee Ligue Contre le Cancer
- Institut Universitaire de France
- INSERM
- CNRS
- Aix-Marseille University
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.
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