| First Author | Qian L | Year | 2019 |
| Journal | J Exp Med | Volume | 216 |
| Issue | 4 | Pages | 884-899 |
| PubMed ID | 30898894 | Mgi Jnum | J:275230 |
| Mgi Id | MGI:6305960 | Doi | 10.1084/jem.20182100 |
| Citation | Qian L, et al. (2019) Suppression of ILC2 differentiation from committed T cell precursors by E protein transcription factors. J Exp Med 216(4):884-899 |
| abstractText | Current models propose that group 2 innate lymphoid cells (ILC2s) are generated in the bone marrow. Here, we demonstrate that subsets of these cells can differentiate from multipotent progenitors and committed T cell precursors in the thymus, both in vivo and in vitro. These thymic ILC2s exit the thymus, circulate in the blood, and home to peripheral tissues. Ablation of E protein transcription factors greatly promotes the ILC fate while impairing B and T cell development. Consistently, a transcriptional network centered on the ZBTB16 transcription factor and IL-4 signaling pathway is highly up-regulated due to E protein deficiency. Our results show that ILC2 can still arise from what are normally considered to be committed T cell precursors, and that this alternative cell fate is restrained by high levels of E protein activity in these cells. Thymus-derived lung ILC2s of E protein-deficient mice show different transcriptomes, proliferative properties, and cytokine responses from wild-type counterparts, suggesting potentially distinct functions. |
