Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 211, Issue 9, Pages 1723-1731Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20140212
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Funding
- Lucille Castori Center for Microbes, Inflammation, and Cancer
- American Society of Hematology Scholar Award
- Searle Scholars Program
- Cancer Research Institute
- National Institutes of Health [R01-095706, R01-HL069929, R01-AI100288, R01-AI080455, R01-AI101406, K08-KHL115355, R01-AI100874]
- Irvington Fellowship of the Cancer Research Institute
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The bZIP transcription factor Nfil3 (also known as E4BP4) is required for the development of natural killer (NK) cells and type 1 innate lymphoid cells (ILC1s). We find that Nfil3 plays a critical role in the development of other mucosal tissue-associated innate lymphocytes. Type 3 ILCs (ILC3s), including lymphoid tissue inducer (LTi)-like cells, are severely diminished in both numbers and function in Nfil3-deficient mice. Using mixed bone marrow chimeric mice, we demonstrate that Nfil3 is critical for normal development of gut-associated ILC3s in a cell-intrinsic manner. Furthermore, Nfil3 deficiency severely compromises intestinal innate immune defense against acute bacterial infection with Citrobacter rodentium and Clostridium difficile. Nfil3 deficiency resulted in a loss of the recently identified ILC precursor, yet conditional ablation of Nfil3 in the NKp46(+) ILC3 subset did not perturb ILC3 numbers, suggesting that Nfil3 is required early during ILC3 development but not for lineage maintenance. Lastly, a marked defect in type 2 ILCs (ILC2s) was also observed in the lungs and visceral adipose tissue of Nfil3-deficient mice, revealing a general requirement for Nfil3 in the development of all ILC lineages.
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