ArticleJournal of virology2008
Control of virus-specific CD8+ T-cell exhaustion and immune-mediated pathology by E3 ubiquitin ligase Cbl-b during chronic viral infection.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Degradation of IKZF1 prevents epigenetic progression of T cell exhaustion in an antigen-specific assay.Cell reports. Medicine · 2024Article
- T-cell exhaustion in immune-mediated inflammatory diseases: New implications for immunotherapy.Frontiers in immunology · 2022Review
- Low-dose IL-2 therapy invigorates CD8+ T cells for viral control in systemic lupus erythematosus.PLoS pathogens · 2021Article
- E3 ubiquitin ligase Casitas B lineage lymphoma-b and its potential therapeutic implications for immunotherapy.Clinical and experimental immunology · 2021Review
- Severely ill COVID-19 patients display impaired exhaustion features in SARS-CoV-2-reactive CD8Science immunology · 2021Article
- Cellular and Molecular Mechanisms of CD8International journal of molecular sciences · 2020Review
- COVID-19 therapy with mesenchymal stromal cells (MSC) and convalescent plasma must consider exosome involvement: Do the exosomes in convalescent plasma antagonize the weak immune antibodies?Journal of extracellular vesicles · 2020Review
- Severely ill COVID-19 patients display augmented functional properties in SARS-CoV-2-reactive CD8bioRxiv : the preprint server for biology · 2020Article
- E3 Ubiquitin Ligases as Immunotherapeutic Target in Atherosclerotic Cardiovascular Disease.Frontiers in cardiovascular medicine · 2020Review
- Chimeric Hemagglutinin-Based Influenza Virus Vaccines Induce Protective Stalk-Specific Humoral Immunity and Cellular Responses in Mice.ImmunoHorizons · 2019Article
- CBLB Constrains Inactivated Vaccine-Induced CD8Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Article
- Scramblase TMEM16F terminates T cell receptor signaling to restrict T cell exhaustion.The Journal of experimental medicine · 2016Article
- The Microbiome, Systemic Immune Function, and Allotransplantation.Clinical microbiology reviews · 2016Review
- Modulation of Immune Cell Functions by the E3 Ligase Cbl-b.Frontiers in oncology · 2015Review
- The Fusion Protein of CTP-HBcAg18-27-Tapasin Mediates the Apoptosis of CD8(+)T Cells and CD8(+) T Cell Response in HLA-A2 Transgenic Mice.Hepatitis monthly · 2014Article
- Clonal exhaustion as a mechanism to protect against severe immunopathology and death from an overwhelming CD8 T cell response.Frontiers in immunology · 2013Article
- FOXO3 regulates the CD8 T cell response to a chronic viral infection.Journal of virology · 2012Article
- Genomic analysis and pathogenic characteristics of lymphocytic choriomeningitis virus strains isolated in Japan.Comparative medicine · 2012Article
- Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
A characteristic feature in the immune response to many persistent viral infections is the dysfunction or deletion of antigen-specific T cells (exhaustion). This down-regulation of virus-specific T-cell response represents a critical control mechanism that exists within T-cell activation pathways to prevent lethal disease by inappropriate responses against disseminating virus infections. However, the molecular mechanisms by which the immune system determines whether to mount a full response to such infections remain largely unexplored. Here, we have established that in the murine lymphocytic choriomeningitis virus (LCMV) model, induction of the T-cell receptor signaling inhibitor molecule E3 ligase Cbl-b is critically involved in this decision. In particular, our data revealed that Cbl-b controls the program responsible for T-cell tolerance (exhaustion) induction during a chronic viral infection. Thus, Cbl-b(-/-) mice infected with a low dose of LCMV Docile mount a strong CD8(+) T-cell response that rapidly clears the infection, and the animals remain healthy; in contrast, down-regulation of the epitope-specific CD8(+) T-cell population in persistently infected Cbl-b(-/-) mice, compared to that in chronically infected B6 mice, was significantly delayed, and this was associated with increased morbidity and eventual death in nearly 20% of the animals. Interestingly, infection of Cbl-b(-/-) mice with a moderate virus dose resulted in rapid death with 100% mortality by 7 to 8 days after infection, caused by a dysregulated antiviral T-cell response, whereas the infected B6 mice survived and remained healthy. In conclusion, our results suggest that Cbl-b is critically involved in T-cell exhaustion and prevention of lethal disease.
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