4.7 Article

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

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JOURNAL OF EXPERIMENTAL MEDICINE
卷 216, 期 4, 页码 884-899

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ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20182100

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  1. National Institutes of Health [1R01AI126851]
  2. Presbyterian Health Foundation
  3. Lew and Myra Ward Chair in Biomedical Research at the Oklahoma Medical Research Foundation

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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.

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