Journal
JOURNAL OF IMMUNOLOGY
Volume 192, Issue 6, Pages 2667-2676Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1302605
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Funding
- National Health and Medical Research Council of Australia [APP1027472]
- Victorian State Government
- Australian Government National Health and Medical Research Council of Australia Independent Research Institutes Infrastructure Support Scheme
- Boehringer Ingelheim
- Austrian Genome Research in Austria initiative
- National Health and Medical Research Council of Australia Career Development Fellowship
- C.J. Martin Fellowship
- Australian Research Council
- Medical Research Council [G0901737] Funding Source: researchfish
- MRC [G0901737] Funding Source: UKRI
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NK cells can be grouped into distinct subsets that are localized to different organs and exhibit a different capacity to secrete cytokines and mediate cytotoxicity. Despite these hallmarks that reflect tissue-specific specialization in NK cells, little is known about the factors that control the development of these distinct subsets. The basic leucine zipper transcription factor Nfil3 (E4bp4) is essential for bone marrow-derived NK cell development, but it is not clear whether Nfil3 is equally important for all NK cell subsets or how it induces NK lineage commitment. In this article, we show that Nfil3 is required for the formation of Eomes-expressing NK cells, including conventional medullary and thymic NK cells, whereas TRAIL(+) Eomes(-) NK cells develop independently of Nfil3. Loss of Nfil3 during the development of bone marrow-derived NK cells resulted in reduced expression of Eomes and, conversely, restoration of Eomes expression in Nfil3(-/-) progenitors rescued NK cell development and maturation. Collectively, these findings demonstrate that Nfil3 drives the formation of mature NK cells by inducing Eomes expression and reveal the differential requirements of NK cell subsets for Nfil3.
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