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

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 and Omid Akbari ()
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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

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: 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.

Date: 2021
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22832-7

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DOI: 10.1038/s41467-021-22832-7

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