ArticlePLoS pathogens2015
PD-L1 Expression on Retrovirus-Infected Cells Mediates Immune Escape from CD8+ T Cell Killing.
Article in PLoS pathogens, 2015. 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 50 papers.
What it found
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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
50 citing papers in PubMed, 66 citations in OpenAlex.
- The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets.Frontiers in immunology · 2026Review
- CD8 T cells mediate immunosurveillance for neoantigen+ epithelial stem cells in the colon.bioRxiv : the preprint server for biology · 2025Article
- PSMD11 facilitates immune escape by recruiting USP14 to modulate the deubiquitinating degradation of PD-L1 in non-small cell lung cancer.Journal of thoracic disease · 2025Article
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- Mathematical modeling indicates that regulatory inhibition of CD8+ T cell cytotoxicity can limit efficacy of IL-15 immunotherapy in cases of high pre-treatment SIV viral load.PLoS computational biology · 2023Article
- Comprehensive immune profiling reveals thatFrontiers in immunology · 2023Article
- Sensitizing immune unresponsive colorectal cancers to immune checkpoint inhibitors through MAVS overexpression.Journal for immunotherapy of cancer · 2022Article
- Mast Cell Activation Triggered by Retrovirus Promotes Acute Viral Infection.Frontiers in microbiology · 2022Article
- Extrafollicular Plasmablasts Present in the Acute Phase of Infections Express High Levels of PD-L1 and Are Able to Limit T Cell Response.Frontiers in immunology · 2022Article
- Role of the PD-1/PD-L1 Pathway in ExperimentalFrontiers in immunology · 2022Article
- Novel Fluorinated Spermine and Small Molecule PEI to Deliver Anti-PD-L1 and Anti-VEGF siRNA for Highly Efficient Tumor Therapy.Pharmaceutics · 2021Article
- Mechanisms of PD-L1 Regulation in Malignant and Virus-Infected Cells.International journal of molecular sciences · 2021Review
- Nanocarrier vaccines for SARS-CoV-2.Advanced drug delivery reviews · 2021Article
- Immunotherapy With Interferon α11, But Not Interferon Beta, Controls Persistent Retroviral Infection.Frontiers in immunology · 2021Article
- TLR5 activation in hepatocytes alleviates the functional suppression of intrahepatic CD8Immunology · 2020Article
- Immune Checkpoints in Viral Infections.Viruses · 2020Review
- Combination immunotherapy with anti-PD-L1 antibody and depletion of regulatory T cells during acute viral infections results in improved virus control but lethal immunopathology.PLoS pathogens · 2020Article
- iCaFrontiers in immunology · 2020Article
- Friend retrovirus studies reveal complex interactions between intrinsic, innate and adaptive immunity.FEMS microbiology reviews · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytotoxic CD8+ T Lymphocytes (CTL) efficiently control acute virus infections but can become exhausted when a chronic infection develops. Signaling of the inhibitory receptor PD-1 is an important mechanism for the development of virus-specific CD8+ T cell dysfunction. However, it has recently been shown that during the initial phase of infection virus-specific CD8+ T cells express high levels of PD-1, but are fully competent in producing cytokines and killing virus-infected target cells. To better understand the role of the PD-1 signaling pathway in CD8+ T cell cytotoxicity during acute viral infections we analyzed the expression of the ligand on retrovirus-infected cells targeted by CTLs. We observed increased levels of PD-L1 expression after infection of cells with the murine Friend retrovirus (FV) or with HIV. In FV infected mice, virus-specific CTLs efficiently eliminated infected target cells that expressed low levels of PD-L1 or that were deficient for PD-L1 but the population of PD-L1high cells escaped elimination and formed a reservoir for chronic FV replication. Infected cells with high PD-L1 expression mediated a negative feedback on CD8+ T cells and inhibited their expansion and cytotoxic functions. These findings provide evidence for a novel immune escape mechanism during acute retroviral infection based on PD-L1 expression levels on virus infected target cells.
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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.