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

• DOI: 10.1084/jem.20182100
• Publication Date: 2019-12-10T19:57:34Z
• Authors: Liangyue Qian; Sandra Bajana; Constantin Georgescu; Vincent Peng; Hong-Cheng Wang; Indra Adrianto; Marco Colonna; Jose Alberola-Ila; Jonathan D. Wren; Xiao-Hong Sun
• Keywords: Innate lymphoid cell; Cell fate determination; Lymphopoiesis

Current models propose that group 2 innate lymphoid cells (ILC2s) are generated in the bone marrow. Here, we demonstrate subsets of these can differentiate from multipotent progenitors and committed T cell precursors thymus, both vivo vitro. These thymic ILC2s exit circulate blood, home to peripheral tissues. Ablation E protein transcription factors greatly promotes ILC fate while impairing B development. Consistently, a transcriptional network centered on ZBTB16 factor IL-4 signaling pathway is highly up-regulated due deficiency. Our results show ILC2 still arise what normally considered be precursors, this alternative restrained by high levels activity cells. Thymus-derived lung protein–deficient mice different transcriptomes, proliferative properties, cytokine responses wild-type counterparts, suggesting potentially distinct functions.