ArticleThe Journal of infectious diseases2017
Selective Destruction of Interleukin 23-Induced Expansion of a Major Antigen-Specific γδ T-Cell Subset in Patients With Tuberculosis.
Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Ferroptosis in Low-Density Neutrophils of Tuberculosis Patients Suppresses Bactericidal Function.Clinical and experimental pharmacology & physiology · 2026Article
- Unconventional Immunotherapies in Cancer: Opportunities and Challenges.Pharmaceuticals (Basel, Switzerland) · 2025Review
- FromFrontiers in immunology · 2025Review
- LncRNA SNHG16 Inhibits IntracellularACS omega · 2024Article
- Functional Analysis of Genes inIndian journal of microbiology · 2024Review
- From Host Defense to Metabolic Signatures: Unveiling the Role of γδ T Cells in Bacterial Infections.Biomolecules · 2024Review
- IFNγ-secreting T cells that highly express IL-2 potently inhibit the growth of intracellularFrontiers in immunology · 2024Article
- Differential expression analysis of miRNAs in macrophage-derived exosomes in the tuberculosis-infected bone microenvironment.Frontiers in microbiology · 2023Article
- Adjunctive Zoledronate + IL-2 administrations enhance anti-tuberculosis Vγ2Vδ2 T-effector populations, and improve treatment outcome of multidrug-resistant tuberculosisEmerging microbes & infections · 2022Article
- γδ T cell exhaustion: Opportunities for intervention.Journal of leukocyte biology · 2022Review
- Cytokine Receptors-Regulators of Antimycobacterial Immune Response.International journal of molecular sciences · 2022Review
- Immune regulation and emerging roles of noncoding RNAs inFrontiers in immunology · 2022Review
- miR-495 Regulates Cellular Reactive Oxygen Species Levels by TargetingInfection and immunity · 2021Article
- MIR337-3p Enhances Mycobacterial Pathogenicity Involving TLR4/MYD88 and STAT3 Signals, Impairing VDR Antimicrobial Response and Fast-Acting Immunity.Frontiers in immunology · 2021Article
- A CD4+CD161+ T-Cell Subset Present in Unexposed Humans, Not Tb Patients, Are Fast Acting Cells That Inhibit the Growth of Intracellular Mycobacteria Involving CD161 Pathway, Perforin, and IFN-γ/Autophagy.Frontiers in immunology · 2021Article
- Genetics and Functional Mechanisms of STAT3 Polymorphisms in Human Tuberculosis.Frontiers in cellular and infection microbiology · 2021Article
- Silencing miR-125b-5p attenuates inflammatory response and apoptosis inhibition in mycobacterium tuberculosis-infected human macrophages by targeting DNA damage-regulated autophagy modulator 2 (DRAM2).Cell cycle (Georgetown, Tex.) · 2020Article
- Review
- Development of a Non-Coding-RNA-based EMT/CSC Inhibitory Nanomedicine for In Vivo Treatment and Monitoring of HCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019Article
- Immunological recovery in patients with pulmonary tuberculosis after intensive phase treatment.The Journal of international medical research · 2018Article
Corrections and comments
- Erratum issuedCorrigendum.2019
Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
A loss of antigen-specific T-cell responses due to defective cytokine signaling during infections has not been reported. We hypothesize that tuberculosis can destroy signaling effects of selective cytokine(s) and induce exhaustion of antigen-specific T cells. To test this hypothesis, mechanistic studies were performed to examine whether and how tuberculosis blocked interleukin 23 (IL-23) and interleukin 2 (IL-2) signaling effects on a major human γδ T-cell subpopulation, phosphoantigen HMBPP-specific Vγ2Vδ2 T cells. IL-23 and IL-2 significantly expanded HMBPP-stimulated Vγ2Vδ2 T cells from subjects with latent tuberculosis infection, and IL-2 synergized the effect of IL-23. IL-23-induced expansion of Vγ2Vδ2 T cells involved STAT3. Surprisingly, patients with tuberculosis exhibited a selective destruction of IL-23-induced expansion of these cells. The tuberculosis-driven destruction of IL-23 signaling coincided with decreases of expression and phosphorylation of STAT3. Interestingly, impairing of STAT3 was linked to marked increases in the microRNAs (miRNAs) hsa-miR-337-3p and hsa-miR-125b-5p in Vγ2Vδ2 T cells from patients with tuberculosis. Downregulation of hsa-miR-337-3p and hsa-miR-125b-5p by miRNA sponges improved IL-23-mediated expansion of Vγ2Vδ2 T cells and restored the ability of these cells to produce anti-tuberculosis cytokines. These results support our hypothesis that tuberculosis can selectively impair a cytokine effect while sparing another and can induce exhaustion of T cells in response to the respective cytokine.
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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.