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Systemic Human ILC Precursors Provide a Substrate for Tissue ILC Differentiation

Ai Ing Lim1, Yan Li2, Silvia Lopez-Lastra3

  • 1Innate Immunity Unit, Institut Pasteur, 75724 Paris, France; Inserm U1223, 75015 Paris, France; Université Paris-Diderot, Sorbonne Paris Cité, 75205 Paris, France.

Cell
|March 12, 2017
PubMed

Innate lymphoid cells (ILCs) represent innate versions of T helper and cytotoxic T cells that differentiate from committed ILC precursors (ILCPs). How ILCPs give rise to mature tissue-resident ILCs remains unclear. Here, we identify circulating and tissue ILCPs in humans that fail to express the transcription factors and cytokine outputs of mature ILCs but have these signature loci in an epigenetically poised configuration. Human ILCPs robustly generate all ILC subsets in vitro and in vivo. While human ILCPs express low levels of retinoic acid receptor (RAR)-related orphan receptor C (RORC) transcripts, these cells are found in RORC-deficient patients and retain potential for EOMES+ natural killer (NK) cells, interferon gamma-positive (IFN-γ+) ILC1s, interleukin (IL)-13+ ILC2s, and for IL-22+, but not for IL-17A+ ILC3s. Our results support a model of tissue ILC differentiation ("ILC-poiesis"), whereby diverse ILC subsets are generated in situ from systemically distributed ILCPs in response to local environmental signals.

Keywords:
cell fatecytokinesdevelopmenthumanized miceinnate lymphoid cellslymphopoiesissignalingsingle cell cloningtranscription factors

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