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

Liangyue Qian, Sandra Bajana, Constantin Georgescu, Vincent Peng, Hong Cheng Wang, Indra Adrianto, Marco Colonna, Jose Alberola-Ila, Jonathan D. Wren, Xiao Hong Sun

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)884-899
Number of pages16
JournalJournal of Experimental Medicine
Volume216
Issue number4
DOIs
StatePublished - Apr 1 2019

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