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CD200–CD200R immune checkpoint engagement regulates ILC2 effector function and ameliorates lung inflammation in asthma

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Listed:
  • Pedram Shafiei-Jahani

    (University of Southern California)

  • Doumet Georges Helou

    (University of Southern California)

  • Benjamin P. Hurrell

    (University of Southern California)

  • Emily Howard

    (University of Southern California)

  • Christine Quach

    (University of Southern California)

  • Jacob D. Painter

    (University of Southern California)

  • Lauriane Galle-Treger

    (University of Southern California)

  • Meng Li

    (University of Southern California)

  • Yong-Hwee Eddie Loh

    (University of Southern California)

  • Omid Akbari

    (University of Southern California)

Abstract

The prevalence of asthma and airway hyperreactivity (AHR) is increasing at an alarming rate. Group 2 innate lymphoid cells (ILC2s) are copious producers of type 2 cytokines, which leads to AHR and lung inflammation. Here, we show that mouse ILC2s express CD200 receptor (CD200R) and this expression is inducible. CD200R engagement inhibits activation, proliferation and type 2 cytokine production, indicating an immunoregulatory function for the CD200–CD200R axis on ILC2s. Furthermore, CD200R engagement inhibits both canonical and non-canonical NF-κB signaling pathways in activated ILC2s. Additionally, we demonstrate both preventative and therapeutic approaches utilizing CD200R engagement on ILC2s, which lead to improved airway resistance, dynamic compliance and eosinophilia. These results show CD200R is expressed on human ILC2s, and its engagement ameliorates AHR in humanized mouse models, emphasizing the translational applications for treatment of ILC2-related diseases such as allergic asthma.

Suggested Citation

  • Pedram Shafiei-Jahani & Doumet Georges Helou & Benjamin P. Hurrell & Emily Howard & Christine Quach & Jacob D. Painter & Lauriane Galle-Treger & Meng Li & Yong-Hwee Eddie Loh & Omid Akbari, 2021. "CD200–CD200R immune checkpoint engagement regulates ILC2 effector function and ameliorates lung inflammation in asthma," Nature Communications, Nature, vol. 12(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22832-7
    DOI: 10.1038/s41467-021-22832-7
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