Journal
NATURE IMMUNOLOGY
Volume 14, Issue 4, Pages 389-395Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2545
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Funding
- National Health and Medical Research Council of Australia
- Sylvia and Charles Viertel Foundation
- Howard Hughes Medical Institute
- Australian Research Council
- Leukaemia Foundation
- American Asthma Foundation
- Medical Research Council
- Victorian State Government Operational Infrastructure Support
- MRC [MC_U105178805] Funding Source: UKRI
- Medical Research Council [MC_U105178805] Funding Source: researchfish
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NKp46(+) innate lymphoid cells (ILCs) serve important roles in regulating the intestinal microbiota and defense against pathogens. Whether NKp46(+) ILCs arise directly from lymphoid tissue-inducer (LTi) cells or represent a separate lineage remains controversial. We report here that the transcription factor 1-bet (encoded by Tbx21) was essential for the development of NKp46(+) ILCs but not of LTi cells or nuocytes. Deficiency in interleukin 22 (IL-22)-producing NKp46(+) ILCs resulted in greater susceptibility of Tbx21(-/-) mice to intestinal infection. Haploinsufficient 1-bet expression resulted in lower expression of the signaling molecule Notch, and Notch signaling was necessary for the transition of LTi cells into NKp46(+) ILCs. Furthermore, NKp46(+) ILCs differentiated solely from the CD4(-) LTi population, not the CD4(+) LTi population. Our results pinpoint the regulation of Notch signaling by 1-bet as a distinct molecular pathway that guides the development of NKp46(+) ILCs.
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