Current models propose that group 2 innate lymphoid cells 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 can exit the thymus, circulate in the blood and home to peripheral tissues.  Ablation of E protein transcription factors greatly promotes the innate lymphoid cell fate at the expense of 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 be generated 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. SOURCE: Jonathan Wrem (Jonathan-Wren@omrf.org) -  OMRF

Pluto Bioinformatics

GSE111518: Suppression of ILC2 differentiation from committed T cell precursors by E protein transcription factors