ArticleImmunity, inflammation and disease2020
PD-1 expression affects cytokine production by ILC2 and is influenced by peroxisome proliferator-activated receptor-γ.
Article in Immunity, inflammation and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- The Mechanistic Role of PPARPPAR research · 2026Review
- The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Metabolic adaptations of ILC2 and Th2 cells in type 2 immunity.Current opinion in immunology · 2024Review
- Case report: Sustained complete remission with all-oral MEPED therapy in a patient with Hodgkin's disease developing resistance to pembrolizumab.Frontiers in pharmacology · 2024Article
- Article
- Mitogen-Activated Protein Kinase and Nuclear Hormone Receptor Crosstalk in Cancer Immunotherapy.International journal of molecular sciences · 2023Review
- The impact of peroxisome proliferator-activated receptor-γ activating angiotensin receptor blocker on outcomes of patients receiving immunotherapy.Cancer medicine · 2023Article
- Obesity control by SHIP inhibition requires pan-paralog inhibition and an intact eosinophil compartment.iScience · 2023Article
- Potential tactics with vitamin D and certain phytochemicals for enhancing the effectiveness of immune-checkpoint blockade therapies.Exploration of targeted anti-tumor therapy · 2023Article
- Heterogeneity of type 2 innate lymphoid cells.Nature reviews. Immunology · 2022Review
- Innate lymphoid cells in colorectal cancer.Scandinavian journal of immunology · 2022Review
- The combination of novel immune checkpoints HHLA2 and ICOSLG: A new system to predict survival and immune features in esophageal squamous cell carcinoma.Genes & diseases · 2022Article
- Role of ILC2s in Solid Tumors: Facilitate or Inhibit?Frontiers in immunology · 2022Review
- Group 2 innate lymphoid cells (ILC2s) are important in typical type 2 immune-mediated diseases and an essential therapeutic target.The Journal of international medical research · 2022Review
- The Role of PPAR-γ in Allergic Disease.Current allergy and asthma reports · 2021Review
- PPARγ induces PD-L1 expression in MSS+ colorectal cancer cells.Oncoimmunology · 2021Article
- PPARɣ drives IL-33-dependent ILC2 pro-tumoral functions.Nature communications · 2021Article
- The devil's in the detail: cell-specific role of PPARγ in ILC2 activation by IL-33.Mucosal immunology · 2021Article
- PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2.Mucosal immunology · 2021Article
- PD-1 Affects the Immunosuppressive Function of Group 2 Innate Lymphoid Cells in Human Non-Small Cell Lung Cancer.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionInnate lymphoid cells (ILCs) can provide early cytokine help against a variety of pathogens in the lungs and gastrointestinal tract. Type 2 ILC (ILC2) are comparable to T helper 2 cells found in the adaptive immune system, which secrete cytokines such as interleukin 5 (IL-5) and IL-13 and have been found to play roles in host defense against helminth infections and in allergic responses. Recent studies have identified that programmed cell death protein 1 (PD-1) and peroxisome proliferator activated receptor-γ (PPAR-γ) are highly expressed by ILC2. We examined whether PD-1 plays a role in ILC2 function and whether there was any connection between PD-1 and PPAR-γ
methodsTo ensure that only innate immune cells were present, ILC2 cells were examined from RAG1
resultsWe found that ILC2 from PD-1
conclusionsThese findings illustrate that chronic loss of PD-1 plays a role in ILC2 function and PD-1 expression can be modulated by PPAR-γ.
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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.