ArticleNature communications2020
PD-1 pathway regulates ILC2 metabolism and PD-1 agonist treatment ameliorates airway hyperreactivity.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
120 citing papers in PubMed.
- PGE2 Enhances Human ILC3 Function but Constrains ILC2-to-ILC3 Plasticity.European journal of immunology · 2026Article
- Realizing the potential of agonistic antibody immunotherapy.Nature reviews. Drug discovery · 2026Review
- Regulation of PD-1PD-L1 Immune Checkpoints by Gut Microbiota Metabolites and Their Clinical Translational Research: A Review.Immunity, inflammation and disease · 2026Review
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- MyD88 mediates allergic airway inflammation by regulating ILC2s function through inducing the formation of P38/GATA3 complex.Respiratory research · 2026Article
- Review
- Acute stress alleviates type 2 lung inflammation by restricting ILC2s through corticosterone-glucocorticoid receptor signaling.Cellular & molecular immunology · 2026Article
- ILC2s and their immune checkpoints in the antitumor response.Journal for immunotherapy of cancer · 2026Review
- Lactate signaling and immune suppression in tumors: mechanisms and therapeutic implications.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Involvement of the PD-1 pathway in the modulation of immune responses during allergic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Tim-3 agonist restrains ILC2 function and attenuates airway hyperreactivity via NLK pathway.Nature communications · 2026Article
- Clinical and Pathophysiological Characteristics of Patients in Whom Asthma Developed during Treatment with Immune Checkpoint Inhibitors: A Retrospective Single-center Study.Internal medicine (Tokyo, Japan) · 2026Article
- Advanced immunotherapy across diseases and the role of artificial intelligence: A review.Biomolecules & biomedicine · 2026Review
- Metabolic licensing at the dendritic cell-NK cells immune synapse in viral asthma exacerbations.Frontiers in immunology · 2026Review
- Hair follicle immune privilege in autoimmune and immune-mediated alopecias: paths toward reestablishing immune tolerance.Frontiers in medicine · 2026Review
- Frequencies of PD-1 and LAG-3 positive T cells in asthmatic children and their relationship with inflammatory cytokines.Open medicine (Warsaw, Poland) · 2026Article
- The Expanding Role of ILC2s in Allergic Airways Disease.Allergy · 2026Review
- Melatonin suppresses ILC2-driven airway hyperreactivity via glutathione-dependent metabolic reprogramming.Frontiers in immunology · 2026Article
- Glycolytic reprogramming and cell-specific lactylation in asthma: an evidence-graded framework for testable metabolic-epigenetic profiles.Frontiers in immunology · 2026Review
- Neuroepithelial VIP-VIPR1 interactions differentially control enteric type 1 and type 2 immunity.Nature immunology · 2025Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.