ArticleJournal of virology2011
Major histocompatibility complex-dependent cytotoxic T lymphocyte repertoire and functional avidity contribute to strain-specific disease susceptibility after murine respiratory syncytial virus infection.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Compensatory relationships determine the impact of TGF-β on the humoral immune response to hepatitis B surface antigen.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- RSV: an overview of infection in adults.Pneumonia (Nathan Qld.) · 2025Review
- mRNA Therapeutic Vaccine for Hepatitis B Demonstrates Immunogenicity and Efficacy in the AAV-HBV Mouse Model.Vaccines · 2024Article
- Neutrophils do not impact viral load or the peak of disease severity during RSV infection.Scientific reports · 2020Article
- LAIR-1 Limits Neutrophilic Airway Inflammation.Frontiers in immunology · 2019Article
- Memory CD8 T cells mediate severe immunopathology following respiratory syncytial virus infection.PLoS pathogens · 2018Article
- Whole Exome Sequencing reveals new candidate genes in host genomic susceptibility to Respiratory Syncytial Virus Disease.Scientific reports · 2017Article
- Host genetics play a critical role in controlling CD8 T cell function and lethal immunopathology during chronic viral infection.PLoS pathogens · 2017Article
- Cellular GFP Toxicity and Immunogenicity: Potential Confounders in in Vivo Cell Tracking Experiments.Stem cell reviews and reports · 2016Review
- Human CD8(+) T Cells Target Multiple Epitopes in Respiratory Syncytial Virus Polymerase.Viral immunology · 2016Article
- Ginseng diminishes lung disease in mice immunized with formalin-inactivated respiratory syncytial virus after challenge by modulating host immune responses.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Article
- Respiratory syncytial virus--a comprehensive review.Clinical reviews in allergy & immunology · 2013Review
- Specific dietary oligosaccharides increase Th1 responses in a mouse respiratory syncytial virus infection model.Journal of virology · 2012Article
- Functional avidity: a measure to predict the efficacy of effector T cells?Clinical & developmental immunology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Susceptibility to respiratory syncytial virus (RSV) infection in mice is genetically determined. While RSV causes little pathology in C57BL/6 mice, pulmonary inflammation and weight loss occur in BALB/c mice. Using major histocompatibility complex (MHC)-congenic mice, we observed that the H-2(d) allele can partially transfer disease susceptibility to C57BL/6 mice. This was not explained by altered viral elimination or differences in the magnitude of the overall virus-specific cytotoxic T lymphocyte (CTL) response. However, H-2(d) mice showed a more focused response, with 70% of virus-specific CTL representing Vβ8.2(+) CTL directed against the immunodominant epitope M2-1 82, while in H-2(b) mice only 20% of antiviral CTL were Vβ9(+) CTL specific for the immunodominant epitope M187. The immunodominant H-2(d)-restricted CTL lysed target cells less efficiently than the immunodominant H-2(b) CTL, probably contributing to prolonged CTL stimulation and cytokine-mediated immunopathology. Accordingly, reduction of dominance of the M2-1 82-specific CTL population by introduction of an M187 response in the F1 generation of a C57BL/6N × C57BL/6-H-2(d) mating (C57BL/6-H-2(dxb) mice) attenuated disease. Moreover, disease in H-2(d) mice was less pronounced after infection with an RSV mutant failing to activate M2-1 82-specific CTL or after depletion of Vβ8.2(+) cells. These data illustrate how the MHC-determined diversity and functional avidity of CTL responses contribute to disease susceptibility after viral infection.
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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.