ArticleViral immunology2008
Generation of a protective T-cell response following coronavirus infection of the central nervous system is not dependent on IL-12/23 signaling.
Article in Viral immunology, 2008. 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.
- Utility and risk of dermatologic medications during the COVID-19 pandemic.Dermatologic therapy · 2020Review
- Infection risk of dermatologic therapeutics during the COVID-19 pandemic: an evidence-based recalibration.International journal of dermatology · 2020Review
- T cell-selective deletion of Oct1 protects animals from autoimmune neuroinflammation while maintaining neurotropic pathogen response.Journal of neuroinflammation · 2019Article
- Epstein-Barr virus-induced gene 3 negatively regulates neuroinflammation and T cell activation following coronavirus-induced encephalomyelitis.Journal of neuroimmunology · 2013Article
- Review
- ssICAM-1, IL-21 and IL-23 in patients with tick borne encephalitis and neuroborreliosis.Cytokine · 2012Article
- UNC93B1 mediates innate inflammation and antiviral defense in the liver during acute murine cytomegalovirus infection.PloS one · 2012Article
- Highly activated cytotoxic CD8 T cells express protective IL-10 at the peak of coronavirus-induced encephalitis.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Impaired immune responses following spinal cord injury lead to reduced ability to control viral infection.Experimental neurology · 2010Article
- The pathogenesis of murine coronavirus infection of the central nervous system.Critical reviews in immunology · 2010Review
- Previous hepatitis a virus infection is related to slower psychomotor speed in elderly adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2009Article
- Inflammatory skin disease in K5.hTGF-beta1 transgenic mice is not dependent on the IL-23/Th17 inflammatory pathway.The Journal of investigative dermatology · 2009Article
- Interleukin-12 (IL-12), but not IL-23, deficiency ameliorates viral encephalitis without affecting viral control.Journal of virology · 2009Article
- The Biology of Persistent Infection: Inflammation and Demyelination following Murine Coronavirus Infection of the Central Nervous System.Current immunology reviews · 2009Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
The functional role of IL-12 and IL-23 in host defense and disease following viral infection of the CNS was determined. Instillation of mouse hepatitis virus (MHV, a positive-strand RNA virus) into the CNS of mice results in acute encephalitis followed by a chronic immune-mediated demyelinating disease. Antibody-mediated blocking of either IL-23 (anti-IL-23p19) or IL-12 and IL-23 (anti-IL-12/23p40) signaling did not mute T-cell trafficking into the CNS or antiviral effector responses and mice were able to control viral replication within the brain. Therapeutic administration of either anti-IL-23p19 or anti-IL-12/23p40 to mice with viral-induced demyelination did not attenuate T-cell or macrophage infiltration into the CNS nor improve clinical disease or diminish white matter damage. In contrast, treatment of mice with anti-IL-12/23p40 or anti-IL-23p19 resulted in inhibition of the autoimmune model of demyelination, experimental autoimmune encephalomyelitis (EAE). These data indicate that (1) IL-12 and IL-23 signaling are dispensable in generating a protective T-cell response following CNS infection with MHV, and (2) IL-12 and IL-23 do not contribute to demyelination in a model independent of autoimmune T-cell-mediated pathology. Therefore, therapeutic targeting of IL-12 and/or IL-23 for the treatment of autoimmune diseases may offer unique advantages by reducing disease severity without muting protective responses following viral infection.
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