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PD-1 pathway regulates ILC2 metabolism and PD-1 agonist treatment ameliorates airway hyperreactivity.

Abstract：

:Allergic asthma is a leading chronic disease associated with airway hyperreactivity (AHR). Type-2 innate lymphoid cells (ILC2s) are a potent source of T-helper 2 (Th2) cytokines that promote AHR and lung inflammation. As the programmed cell death protein-1 (PD-1) inhibitory axis regulates a variety of immune responses, here we investigate PD-1 function in pulmonary ILC2s during IL-33-induced airway inflammation. PD-1 limits the viability of ILC2s and downregulates their effector functions. Additionally, PD-1 deficiency shifts ILC2 metabolism toward glycolysis, glutaminolysis and methionine catabolism. PD-1 thus acts as a metabolic checkpoint in ILC2s, affecting cellular activation and proliferation. As the blockade of PD-1 exacerbates AHR, we also develop a human PD-1 agonist and show that it can ameliorate AHR and suppresses lung inflammation in a humanized mouse model. Together, these results highlight the importance of PD-1 agonistic treatment in allergic asthma and underscore its therapeutic potential.

journal_name

Nat Commun

journal_title

Nature communications

authors

Helou DG,Shafiei-Jahani P,Lo R,Howard E,Hurrell BP,Galle-Treger L,Painter JD,Lewis G,Soroosh P,Sharpe AH,Akbari O

doi

10.1038/s41467-020-17813-1

subject

Has Abstract

pub_date

2020-08-10 00:00:00

pages

3998

issue

1

issn

2041-1723

pii

10.1038/s41467-020-17813-1

journal_volume

11

pub_type

杂志文章

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