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The effector fates of innate lymphoid cells (ILCs) are epigenetically imprinted early in ontogeny through the selective loss of DNA methylation at signature genes encoding fate-determining regulators — a process that is important for functional diversification of barrier immunity.
Correction to: Nature Immunology https://doi.org/10.1038/s41590-024-01807-y, published online 17 April 2024 In the version of the article initially published, in the RUNX1 cKO ETP row of Fig. 3h, the range now reading 0–11 originally read 0–1 and has now been amended in the HTML and PDF versions of the article. About this article Gamble, N., Bradu, A., Caldwell, J.A. et al.
Abstract Adaptive immunity relies on specialized effector functions elicited by lymphocytes, yet how antigen recognition activates appropriate effector responses through nonspecific signaling intermediates is unclear. Here we examined the role of chromatin priming in specifying the functional outputs of effector T cells and found that most of the cis-regulatory landscape active in effector T cells was poised early in development before the expression of the T cell antigen receptor.
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