ArticleEuropean journal of immunology2014
Phosphorylated STAT3 and PD-1 regulate IL-17 production and IL-23 receptor expression in Mycobacterium tuberculosis infection.
Article in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Anti-PD-L1 Therapy Does Not Improve Survival in a Murine Model of Lethal Staphylococcus aureus Pneumonia.The Journal of infectious diseases · 2021Pooled it
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Identification and validation of NETs-related biomarkers in active tuberculosis through bioinformatics analysis and machine learning algorithms.Frontiers in immunology · 2025Article
- 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
- Immune mechanisms of granuloma formation in sarcoidosis and tuberculosis.The Journal of clinical investigation · 2024Review
- Overexpression of LAG-3: a potential indicator of low immune function in tuberculosis.Frontiers in cellular and infection microbiology · 2024Article
- PD-1 and TIM-3 differentially regulate subsets of mouse IL-17A-producing γδ T cells.The Journal of experimental medicine · 2023Article
- In vitro characterization of a small molecule PD-1 inhibitor that targets the PD-l/PD-L1 interaction.Scientific reports · 2022Article
- Chronic Pulmonary Aspergillosis: Disease Severity Using Image Analysis and Correlation with Systemic Proinflammation and Predictors of Clinical Outcome.Journal of fungi (Basel, Switzerland) · 2021Article
- Genetics and Functional Mechanisms of STAT3 Polymorphisms in Human Tuberculosis.Frontiers in cellular and infection microbiology · 2021Article
- Constitutive STAT3 phosphorylation and IL-6/IL-10 co-expression are associated with impaired T-cell function in tuberculosis patients.Cellular & molecular immunology · 2019Article
- Sputum Detection of Predisposing Genetic Mutations in Women with Pulmonary Nontuberculous Mycobacterial Disease.Scientific reports · 2018Article
- IL-17 and IL-22 production in HIV+ individuals with latent and active tuberculosis.BMC infectious diseases · 2018Article
- The crucial roles of Th17-related cytokines/signal pathways in M. tuberculosis infection.Cellular & molecular immunology · 2018Review
- Pharmacokinetic and Pharmacodynamic Considerations for the Use of Monoclonal Antibodies in the Treatment of Bacterial Infections.Antibodies (Basel, Switzerland) · 2018Review
- Decreased T helper 17 cells in tuberculosis is associated with increased percentages of programmed death ligand 1, T helper 2 and regulatory T cells.Respiratory research · 2017Article
- Reduced T-Helper 17 Responses to Streptococcus pneumoniae in Infection-Prone Children Can Be Rescued by Addition of Innate Cytokines.The Journal of infectious diseases · 2017Article
- Selective Destruction of Interleukin 23-Induced Expansion of a Major Antigen-Specific γδ T-Cell Subset in Patients With Tuberculosis.The Journal of infectious diseases · 2017Article
- The immunomodulatory effects of TNF-α inhibitors on human Th17 cells via RORγt histone acetylation.Oncotarget · 2017Article
- Disseminated Tuberculosis and Chronic Mucocutaneous Candidiasis in a Patient with a Gain-of-Function Mutation in Signal Transduction and Activator of Transcription 1.Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
We studied the factors that regulate IL-23 receptor expression and IL-17 production in human tuberculosis infection. Mycobacterium tuberculosis (M. tb)-stimulated CD4(+) T cells from tuberculosis patients secreted less IL-17 than did CD4(+) T cells from healthy tuberculin reactors (PPD(+) ). M. tb-cultured monocytes from tuberculosis patients and PPD(+) donors expressed equal amounts of IL-23p19 mRNA and protein, suggesting that reduced IL-23 production is not responsible for decreased IL-17 production by tuberculosis patients. Freshly isolated and M. tb-stimulated CD4(+) T cells from tuberculosis patients had reduced IL-23 receptor and phosphorylated STAT3 (pSTAT3) expression, compared with cells from PPD(+) donors. STAT3 siRNA reduced IL-23 receptor expression and IL-17 production by CD4(+) T cells from PPD(+) donors. Tuberculosis patients had increased numbers of PD-1(+) T cells compared with healthy PPD(+) individuals. Anti-PD-1 antibody enhanced pSTAT3 and IL-23R expression and IL-17 production by M. tb-cultured CD4(+) T cells of tuberculosis patients. Anti-tuberculosis therapy decreased PD-1 expression, increased IL-17 and IFN-γ production and pSTAT3 and IL-23R expression. These findings demonstrate that increased PD-1 expression and decreased pSTAT3 expression reduce IL-23 receptor expression and IL-17 production by CD4(+) T cells of tuberculosis patients.
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