ArticleJournal of immunology (Baltimore, Md. : 1950)2015
NF-κB regulates PD-1 expression in macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.
What it found
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The trial behind it
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Who cites it
109 citing papers in PubMed, 163 citations in OpenAlex.
- Lenalidomide triggers T-cell effector functions in vivo in patients with follicular lymphoma.Blood advances · 2021Trial
- PD-L1Haematologica · 2018Trial
- PD-1⁺ CD8⁺ T cells: roles of PD-1 beyond an exhaustion marker.Seminars in immunopathology · 2026Review
- Insight of immune checkpoint blockades in melanoma: mechanism and clinical translation.Molecular cancer · 2026Review
- The role of programmed cell death 1 in autoimmune diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Physical activity attenuates PD-1/PD-L1 expression and enhances CD4⁺ T-cell function in COPD patients.Scientific reports · 2025Article
- The role of coinhibitory receptor-expressing non-T cells in inflammation and immunity: unsung heroes or peripheral players?Experimental & molecular medicine · 2025Review
- High-plex imaging of hepatoblastoma and adjacent liver in pediatric patients reveals a predominant myeloid infiltrate expressing immune-checkpoints.Cancer immunology, immunotherapy : CII · 2025Article
- Review
- Tumor microenvironment noise-induced polarization: the main challenge in macrophages' immunotherapy for cancer.Molecular and cellular biochemistry · 2025Review
- Lidocaine Modulates Cytokine Production and Reprograms the Tumor Immune Microenvironment to Enhance Anti-Tumor Immune Responses in Gastric Cancer.International journal of molecular sciences · 2025Article
- Immune checkpoint blockade for cancer therapy: current progress and perspectives.Journal of Zhejiang University. Science. B · 2025Review
- The Novel Role of the Expression of Toll-like Receptors TLR-5, TLR-6, and TLR-9 and Associated Up-Regulation of Programmed Cell Death 1 Receptor (PD-1) and Its Ligand (PD-L1) in Lung Sepsis.International journal of molecular sciences · 2025Article
- Post-translational governance of NF-κB in cancer immunity: mechanisms and therapeutic horizons.Frontiers in immunology · 2025Review
- Targeting of TAMs: can we be more clever than cancer cells?Cellular & molecular immunology · 2024Review
- Monocyte programmed death-ligand 1 upregulation in early post-out-of-hospital cardiac arrest is associated with increased risk of acute respiratory distress syndrome.Resuscitation plus · 2024Article
- The Potential of PD-1 and PD-L1 as Prognostic and Predictive Biomarkers in Colorectal Adenocarcinoma Based on TILs Grading.Current oncology (Toronto, Ont.) · 2024Article
- Article
- Regulatory mechanisms of PD-1/PD-L1 in cancers.Molecular cancer · 2024Review
- Engineering PD-1-targeted small protein variants for in vitro diagnostics and in vivo PET imaging.Journal of translational medicine · 2024Article
49 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
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Programmed cell death-1 (PD-1) is responsible for T cell exhaustion during chronic viral infections and is expressed on a variety of immune cells following activation. Despite its importance, the mechanisms that regulate PD-1 in cell types other than CD8 T cells are poorly defined. In this study, the molecular mechanisms for inducing PD-1 expression in CD4 T cells, macrophages, and B cells were explored. In CD4 T cells, PD-1 induction following TCR stimulation required NFAT, as the calcineurin/NFAT pathway inhibitor cyclosporin A was able to block PD-1 induction in a manner similar to that seen in CD8 T cells. In contrast, LPS but not PMA and ionomycin stimulation was able to induce PD-1 expression in macrophages in a manner insensitive to cyclosporin A-mediated inhibition. B cells could use both pathways, although the levels of PD-1 expression were highest with PMA and ionomycin. An NF-κB binding site located upstream of the gene in conserved region C was required for NF-κB-dependent PD-1 gene activation in macrophages. Chromatin immunoprecipitation showed NF-κB p65 binding to this region following stimulation of macrophages with LPS. PD-1 induction was associated with histone modifications characteristic of accessible chromatin; however, in contrast to CD8 T cells, conserved region B in macrophages did not lose CpG methylation upon stimulation and PD-1 expression. The linkage of TLR/NF-κB signaling to the induction of PD-1 suggests the possibility of an opportunistic advantage to microbial infections in manipulating immune inhibitory responses.
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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.