ArticleThe Journal of clinical investigation2010
Tim-3 expression on PD-1+ HCV-specific human CTLs is associated with viral persistence, and its blockade restores hepatocyte-directed in vitro cytotoxicity.
Article in The Journal of clinical investigation, 2010. 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 186 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
186 citing papers in PubMed, 1 synthesis or guideline pooled it.
- An Emerging Role of TIM3 Expression on T Cells in Chronic Kidney Inflammation.Frontiers in immunology · 2021Pooled it
- Longitudinal assessment of T cell inhibitory receptors in liver transplant recipients and their association with posttransplant infections.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018Trial
- Trial
- Enhanced suppressor function of TIM-3+ FoxP3+ regulatory T cells.European journal of immunology · 2014Trial
- Trial
- Enhanced virus-specific CD8+ T cell responses by Listeria monocytogenes-infected dendritic cells in the context of Tim-3 blockade.PloS one · 2014Trial
- Galectin-9 and IL-21 mediate cross-regulation between Th17 and Treg cells during acute hepatitis C.PLoS pathogens · 2013Trial
- Tim-3-expressing CD4+ and CD8+ T cells in human tuberculosis (TB) exhibit polarized effector memory phenotypes and stronger anti-TB effector functions.PLoS pathogens · 2012Trial
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Breakthroughs in HBV-related HCC Therapy: The Unmatched Potential of Immune Checkpoint Inhibitors.Current treatment options in oncology · 2026Review
- Blockade of Tim-3 pathway in a mouse model of Toxoplasmosis: impact on brain leukocyte infiltration, parasite burden, and neuroinflammation.Scientific reports · 2026Article
- T cell dysfunction and metabolic disruption in chronic hepatitis C virus infection.Frontiers in immunology · 2026Review
- Tim-3 Is Required for Regulatory T Cell-Mediated Promotion of T Cell Exhaustion and Viral Persistence during Chronic Lymphocytic Choriomeningitis Virus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Evaluation of changes in exhausted T lymphocytes and miRNAs expression in the different trimesters of pregnancy in pregnant women.Molecular biology reports · 2024Article
- Dysfunction and regulatory interplay of T and B cells in chronic hepatitis B: immunotherapy and emerging antiviral strategies.Frontiers in cellular and infection microbiology · 2024Review
- Role of TIM-3 in ovarian cancer: the forsaken cop or a new noble.Frontiers in immunology · 2024Review
- Article
- Polymorphisms Related to Iron Homeostasis Associate with Liver Disease in Chronic Hepatitis C.Viruses · 2023Article
- Role of Tim-3 in COVID-19: a potential biomarker and therapeutic target.Archives of virology · 2023Review
- Double Positive CD4Cells · 2023Article
126 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
Having successfully developed mechanisms to evade immune clearance, hepatitis C virus (HCV) establishes persistent infection in approximately 75%-80% of patients. In these individuals, the function of HCV-specific CD8+ T cells is impaired by ligation of inhibitory receptors, the repertoire of which has expanded considerably in the past few years. We hypothesized that the coexpression of the negative regulatory receptors T cell immunoglobulin and mucin domain-containing molecule 3 (Tim-3) and programmed death 1 (PD-1) in HCV infection would identify patients at risk of developing viral persistence during and after acute HCV infection. The frequency of PD-1-Tim-3- HCV-specific CTLs greatly outnumbered PD-1+Tim-3+ CTLs in patients with acute resolving infection. Moreover, the population of PD-1+Tim-3+ T cells was enriched for within the central memory T cell subset and within the liver. Blockade of either PD-1 or Tim-3 enhanced in vitro proliferation of HCV-specific CTLs to a similar extent, whereas cytotoxicity against a hepatocyte cell line that expressed cognate HCV epitopes was increased exclusively by Tim-3 blockade. These results indicate that the coexpression of these inhibitory molecules tracks with defective T cell responses and that anatomical differences might account for lack of immune control of persistent pathogens, which suggests their manipulation may represent a rational target for novel immunotherapeutic approaches.
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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.