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Alternative activation generates IL-10 producing type 2 innate lymphoid cells

Author

Listed:
  • Corey R. Seehus

    (Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center)

  • Asha Kadavallore

    (Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center)

  • Brian de la Torre

    (Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center)

  • Alyson R. Yeckes

    (Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center)

  • Yizhou Wang

    (Cedars-Sinai Medical Center)

  • Jie Tang

    (Cedars-Sinai Medical Center)

  • Jonathan Kaye

    (Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center
    David Geffen School of Medicine, University of California, Los Angeles)

Abstract

Type 2 innate lymphoid cells (ILC2) share cytokine and transcription factor expression with CD4+ Th2 cells, but functional diversity of the ILC2 lineage has yet to be fully explored. Here, we show induction of a molecularly distinct subset of activated lung ILC2, termed ILC210. These cells produce IL-10 and downregulate some pro-inflammatory genes. Signals that generate ILC210 are distinct from those that induce IL-13 production, and gene expression data indicate that an alternative activation pathway leads to the generation of ILC210. In vivo, IL-2 enhances ILC210 generation and is associated with decreased eosinophil recruitment to the lung. Unlike most activated ILC2, the ILC210 population contracts after cessation of stimulation in vivo, with maintenance of a subset that can be recalled by restimulation, analogous to T-cell effector cell and memory cell generation. These data demonstrate the generation of a previously unappreciated IL-10 producing ILC2 effector cell population.

Suggested Citation

  • Corey R. Seehus & Asha Kadavallore & Brian de la Torre & Alyson R. Yeckes & Yizhou Wang & Jie Tang & Jonathan Kaye, 2017. "Alternative activation generates IL-10 producing type 2 innate lymphoid cells," Nature Communications, Nature, vol. 8(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-02023-z
    DOI: 10.1038/s41467-017-02023-z
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