ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Persistent viral infection elevates central nervous system MHC class I through chronic production of interferons.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 18 citations in OpenAlex.
- Immunotherapeutic benefit of α-interferon (IFNα) in survivin2B-derived peptide vaccination for advanced pancreatic cancer patients.Cancer science · 2013Trial
- How persistent infection overcomes peripheral tolerance mechanisms to cause T cell-mediated autoimmune disease.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Microglial MHC-I induction with aging and Alzheimer's is conserved in mouse models and humans.GeroScience · 2023Article
- Microglial MHC-I induction with aging and Alzheimer's is conserved in mouse models and humans.bioRxiv : the preprint server for biology · 2023Article
- Alcohol intake alters immune responses and promotes CNS viral persistence in mice.Behavioural brain research · 2016Article
- Pre-Natal Exposure to Mouse Parvovirus at Day 5 and 12 Gestation Does Not Induce Immune Tolerance.PloS one · 2016Article
- Characteristics and critical function of CD8+ T cells in the Toxoplasma-infected brain.Seminars in immunopathology · 2015Review
- Distinct neural stem cell tropism, early immune activation, and choroid plexus pathology following coxsackievirus infection in the neonatal central nervous system.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- The great balancing act: regulation and fate of antiviral T-cell interactions.Immunological reviews · 2013Review
- Role of antigen persistence and dose for CD4+ T-cell exhaustion and recovery.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Article
- Viperin is highly induced in neutrophils and macrophages during acute and chronic lymphocytic choriomeningitis virus infection.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Type I interferon modulates the battle of host immune system against viruses.Advances in applied microbiology · 2010Review
- Neurons under viral attack: victims or warriors?Neurochemistry internationalReview
- Neuronal expression of β2M and MHC I are essential for peripheral surveillance and targeting of neuron-restricted antigens.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Persistence of even the stealthiest viruses can perturb immune function either to the benefit or detriment of the host. Lymphocytic choriomeningitis virus (LCMV) establishes lifelong, systemic persistence when introduced in utero or at birth. Despite a highly evolved host-pathogen relationship, LCMV cannot escape detection by the innate immune system, which results in chronic stimulation of the type 1 IFN pathway in adult carrier mice. In this study we demonstrate that IFN-beta is chronically up-regulated in peripheral lymphoid and nonlymphoid tissues (but not the CNS) of mice persistently infected from birth with LCMV and that dendritic cells (DCs) represent at least one source of IFN-beta. Interestingly, chronic stimulation of this innate pathway significantly elevated MHC class I expression in the CNS as well as the periphery. Elevated MHC I expression was dependent on IFN-alphabeta receptor but not MyD88-dependent signaling, as only genetic deletion of the former reduced MHC I to normal levels. An increase in circulating virus was also observed in the IFN-alphabeta receptor deficient carrier mice, signifying that type I IFN continually exerts anti-viral pressure during a LCMV carrier state. Finally, to determine whether heightened CNS MHC I could be therapeutically corrected, we purged LCMV carrier mice of their persistent infection using adoptive immunotherapy. This treatment significantly reduced CNS MHC I expression. Collectively, these data demonstrate that even a well adapted pathogen can chronically stimulate the innate immune system and consequently alter the expression of Ag presenting machinery in an immunologically specialized compartment like the CNS.
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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.