ArticleJournal of virology2008
NKG2D receptor signaling enhances cytolytic activity by virus-specific CD8+ T cells: evidence for a protective role in virus-induced encephalitis.
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 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Identification of gene expression signatures associated with neuroinflammation in discogenic sciatica using machine learning and experimental validation.Frontiers in genetics · 2026Article
- The HHV-6A Proteins U20 and U21 Target NKG2D Ligands to Escape Immune Recognition.Frontiers in immunology · 2021Article
- Functions of NKG2D in CD8Cellular & molecular immunology · 2018Review
- Activating receptor NKG2D targets RAE-1-expressing allogeneic neural precursor cells in a viral model of multiple sclerosis.Stem cells (Dayton, Ohio) · 2014Article
- Influenza infection results in local expansion of memory CD8(+) T cells with antigen non-specific phenotype and function.Clinical and experimental immunology · 2014Article
- Review
- MHC mismatch results in neural progenitor cell rejection following spinal cord transplantation in a model of viral-induced demyelination.Stem cells (Dayton, Ohio) · 2012Article
- Regulation of immune cell function and differentiation by the NKG2D receptor.Cellular and molecular life sciences : CMLS · 2011Review
- mTOR kinase inhibitor AZD8055 enhances the immunotherapeutic activity of an agonist CD40 antibody in cancer treatment.Cancer research · 2011Article
- Manipulation of NKG2D ligands by cytomegaloviruses: impact on innate and adaptive immune response.Frontiers in immunology · 2011Article
- CXCR2 signaling protects oligodendrocytes and restricts demyelination in a mouse model of viral-induced demyelination.PloS one · 2010Article
- Effect of NKG2D ligand expression on host immune responses.Immunological reviews · 2010Review
- Treatment with a sphingosine analog does not alter the outcome of a persistent virus infection.Virology · 2010Article
- The pathogenesis of murine coronavirus infection of the central nervous system.Critical reviews in immunology · 2010Review
- A protective role for ELR+ chemokines during acute viral encephalomyelitis.PLoS pathogens · 2009Article
- Functional characterization of mouse spinal cord infiltrating CD8+ lymphocytes.Journal of neuroimmunology · 2009Article
- The Biology of Persistent Infection: Inflammation and Demyelination following Murine Coronavirus Infection of the Central Nervous System.Current immunology reviews · 2009Article
- Neuroimmunology of central nervous system viral infections: the cells, molecules and mechanisms involved.Current opinion in pharmacology · 2008Review
- DNAX-activating protein 10 co-stimulation enhances the anti-tumor efficacy of chimeric antigen receptor T cells.OncoimmunologyArticle
- Regulation of NKG2DOncoimmunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Inoculation with the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of mice results in an acute encephalitis associated with an immune-mediated demyelinating disease. During acute disease, infiltrating CD8(+) T cells secrete gamma interferon (IFN-gamma) that controls replication in oligodendrocytes, while infected astrocytes and microglia are susceptible to perforin-mediated lysis. The present study was undertaken to reveal the functional contributions of the activating NKG2D receptor in host defense and disease following JHMV infection. NKG2D ligands RAE-1, MULT1, and H60 were expressed within the CNS following JHMV infection. The immunophenotyping of infiltrating cells revealed that NKG2D was expressed on approximately 90% of infiltrating CD8(+) T cells during acute and chronic disease. Blocking NKG2D following JHMV infection resulted in increased mortality that correlated with increased viral titers within the CNS. Anti-NKG2D treatment did not alter T-cell infiltration into the CNS or the generation of virus-specific CD8(+) T cells, and the expression of IFN-gamma was not affected. However, cytotoxic T-lymphocyte (CTL) activity was dependent on NKG2D expression, because anti-NKG2D treatment resulted in a dramatic reduction in lytic activity by virus-specific CD8(+) T cells. Blocking NKG2D during chronic disease did not affect either T-cell or macrophage infiltration or the severity of demyelination, indicating that NKG2D does not contribute to virus-induced demyelination. These findings demonstrate a functional role for NKG2D in host defense during acute viral encephalitis by selectively enhancing CTL activity by infiltrating virus-specific CD8(+) T 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.