Journal
IMMUNITY
Volume 44, Issue 1, Pages 103-115Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2015.12.007
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Funding
- National Health and Medical Research Council (NH&MRC) of Australia [1027472, 1047903, 1016647, 1049407, 1066770, 1057852]
- National Health and Medical Research Council of Australia [GNT0461276, 1058344, 545952]
- Australian Research Council
- Cancer Australia
- Menzies Foundation
- Leukaemia Foundation scholarship
- European Research Council (THINK Advanced Grant)
- INSERM
- CNRS
- Aix Marseille
- Boehringer Ingelheim
- ERC Advanced Grant (Lymphocyte Control) from the European Community's Seventh Framework Program [291740]
- [628623]
- Grants-in-Aid for Scientific Research [15K19547] Funding Source: KAKEN
- European Research Council (ERC) [291740] Funding Source: European Research Council (ERC)
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The inhibitor of DNA binding 2 (Id2) is essential for natural killer (NK) cell development with its canonical role being to antagonize E-protein function and alternate lineage fate. Here we have identified a key role for Id2 in regulating interleukin-15 (IL-15) receptor signaling and homeostasis of NK cells by repressing multiple E-protein target genes including Socs3. Id2 deletion in mature NK cells was incompatible with their homeostasis due to impaired IL-15 receptor signaling and metabolic function and this could be rescued by strong IL-15 receptor stimulation or genetic ablation of Socs3. During NK cell maturation, we observed an inverse correlation between E-protein target genes and Id2. These results shift the current paradigm on the role of ID2, indicating that it is required not only to antagonize E-proteins during NK cell commitment, but constantly required to titrate E-protein activity to regulate NK cell fitness and responsiveness to IL-15.
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