| First Author | Rankin LC | Year | 2013 |
| Journal | Nat Immunol | Volume | 14 |
| Issue | 4 | Pages | 389-95 |
| PubMed ID | 23455676 | Mgi Jnum | J:194819 |
| Mgi Id | MGI:5474876 | Doi | 10.1038/ni.2545 |
| Citation | Rankin LC, et al. (2013) The transcription factor T-bet is essential for the development of NKp46(+) innate lymphocytes via the Notch pathway. Nat Immunol 14(4):389-95 |
| abstractText | 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. |
