ArticlePloS one2015
PD-1, PD-L1 and PD-L2 Gene Expression on T-Cells and Natural Killer Cells Declines in Conjunction with a Reduction in PD-1 Protein during the Intensive Phase of Tuberculosis Treatment.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 62 citations in OpenAlex.
- PDCD1 Signaling in Microglia Can Reduce Neuroinflammation and Apoptosis Induced by Traumatic Brain Injury by Regulating PI3K/Akt Signaling Pathway, Thereby Alleviating Neurological Dysfunction.Molecular neurobiology · 2026Article
- Regulatory Mechanisms of Co-Inhibitory Receptors in Tuberculosis Immunity: Implications for Therapeutic Targets.ImmunoTargets and therapy · 2025Review
- Identification and validation of NETs-related biomarkers in active tuberculosis through bioinformatics analysis and machine learning algorithms.Frontiers in immunology · 2025Article
- Deciphering the Correlation between the Emergence of Lung Carcinoma Associated with Tuberculosis-related Inflammation.Endocrine, metabolic & immune disorders drug targets · 2025Review
- A narrative review of the controversy on the risk of mycobacterial infections with immune checkpoint inhibitor use: does Goldilocks have the answer?Journal of thoracic disease · 2024Review
- PD-L1 Downregulation and DNA Methylation Inhibition for Molecular Therapy against Cancer Stem Cells in Hepatocellular Carcinoma.International journal of molecular sciences · 2023Article
- Eleven Crucial Pesticides Appear to Regulate Key Genes That Link MPTP Mechanism to Cause Parkinson's Disease through the Selective Degeneration of Dopamine Neurons.Brain sciences · 2023Article
- Upregulation of programmed cell death 1 by interferon gamma and its biological functions in human monocytes.Biochemistry and biophysics reports · 2022Article
- The paradox of immune checkpoint inhibition re-activating tuberculosis.The European respiratory journal · 2022Review
- Mycobacterium tuberculosis exploits MPT64 to generate myeloid-derived suppressor cells to evade the immune system.Cellular and molecular life sciences : CMLS · 2022Article
- Natural killer cells and immune-checkpoint inhibitor therapy: Current knowledge and new challenges.Molecular therapy oncolytics · 2022Review
- In vitro characterization of a small molecule PD-1 inhibitor that targets the PD-l/PD-L1 interaction.Scientific reports · 2022Article
- PD-1/PD-L1 Correlates With the Efficacy of the Treatment of Concurrent Chemoradiotherapy in Cervical Cancer.Frontiers in oncology · 2022Article
- Readministration of Pembrolizumab after Treatment of Tuberculosis Activated by Initial Pembrolizumab Therapy.Internal medicine (Tokyo, Japan) · 2021Article
- Programmed cell death-1/programmed cell death-ligand 1 inhibitors exert antiapoptosis and antiinflammatory activity in lipopolysaccharide stimulated murine alveolar macrophages.Experimental and therapeutic medicine · 2021Article
- Clonal Expansion of Tumor-Infiltrating T Cells and Analysis of the Tumor Microenvironment within Esophageal Squamous Cell Carcinoma Relapsed after Definitive Chemoradiation Therapy.International journal of molecular sciences · 2021Article
- Immune checkpoint: The novel target for antitumor therapy.Genes & diseases · 2021Review
- PDL1 expression on monocytes is associated with plasma cytokines in Tuberculosis and HIV.PloS one · 2021Article
- Characterization of Surface Receptor Expression and Cytotoxicity of Human NK Cells and NK Cell Subsets in Overweight and Obese Humans.Frontiers in immunology · 2020Article
- CD163Clinical and experimental dental research · 2019Observational
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe PD-1 axis is a cell intrinsic immunoregulatory pathway that mediates T cell exhaustion in chronic infection particularly in some viral infections. We hypothesized that PD-1, PD-L1 and PD-L2 would be highly expressed in untreated tuberculosis patients compared to controls due to their chronic infection and would decrease with successful TB treatment. MATERIALS AND
methodsUntreated tuberculosis patients (n = 26) were recruited at diagnosis and followed up during treatment. Household contacts (n = 24) were recruited to establish baseline differences. Blood gene expression ex vivo was investigated using qRT-PCR. Flow cytometry was performed to establish protein expression patterns.
resultsPD-L1 gene expression was found to be elevated in active TB disease; however, this was not observed for PD-1 or PD-L2. The intensive phase of TB treatment was associated with a significant decline in PD-1, PD-L1 and PD-L2 gene expression. PD-1 protein expression on the surface of NK cells, CD8+ and CD4+ T cells was similar in patients with active TB disease compared to controls but declined with successful TB treatment, with the greatest decline occurring on the NK cells followed by CD8+ T cells and then CD4+ T cells. Granzyme B/PD-1 co-expression declined with successful intensive phase treatment.
conclusionModulation of PD-1/PD-L1 pathway through TB treatment indicates changes in the peripheral T cell response caused by live Mycobacterium tuberculosis (Mtb) followed by the response to dead bacilli, antigen-release and immuno-pathology resolution. The PD-1 axis could be a host drug target for immunomodulatory treatments in the future.
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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.