Title |
The transcription factor T-bet is essential for the development of NKp46+ innate lymphocytes via the Notch pathway
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Published in |
Nature Immunology, March 2013
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DOI | 10.1038/ni.2545 |
Pubmed ID | |
Authors |
Lucille C Rankin, Joanna R Groom, Michaël Chopin, Marco J Herold, Jennifer A Walker, Lisa A Mielke, Andrew N J McKenzie, Sebastian Carotta, Stephen L Nutt, Gabrielle T Belz |
Abstract |
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 T-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 T-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 T-bet as a distinct molecular pathway that guides the development of NKp46+ ILCs. |
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Country | Count | As % |
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Australia | 2 | 11% |
Germany | 1 | 6% |
Spain | 1 | 6% |
United Kingdom | 1 | 6% |
Unknown | 3 | 17% |
Demographic breakdown
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Science communicators (journalists, bloggers, editors) | 1 | 6% |
Mendeley readers
Geographical breakdown
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Germany | 2 | <1% |
France | 1 | <1% |
Japan | 1 | <1% |
United Kingdom | 1 | <1% |
Unknown | 220 | 96% |
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Readers by professional status | Count | As % |
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Researcher | 51 | 22% |
Student > Master | 23 | 10% |
Student > Bachelor | 16 | 7% |
Other | 16 | 7% |
Other | 32 | 14% |
Unknown | 27 | 12% |
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Chemistry | 4 | 2% |
Other | 13 | 6% |
Unknown | 27 | 12% |