|  Help  |  About  |  Contact Us

Publication : CD200-CD200R immune checkpoint engagement regulates ILC2 effector function and ameliorates lung inflammation in asthma.

First Author  Shafiei-Jahani P Year  2021
Journal  Nat Commun Volume  12
Issue  1 Pages  2526
PubMed ID  33953190 Mgi Jnum  J:337332
Mgi Id  MGI:6713787 Doi  10.1038/s41467-021-22832-7
Citation  Shafiei-Jahani P, et al. (2021) CD200-CD200R immune checkpoint engagement regulates ILC2 effector function and ameliorates lung inflammation in asthma. Nat Commun 12(1):2526
abstractText  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-kappaB 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.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

9 Bio Entities

Trail: Publication

0 Expression