ArticleThe American journal of pathology2004
Cerebral expression of interleukin-12 induces neurological disease via differential pathways and recruits antigen-specific T cells in virus-infected mice.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Age-dependent Powassan virus lethality is linked to glial cell activation and divergent neuroinflammatory cytokine responses in a murine model.Journal of virology · 2024Article
- Tumor Necrosis Factor-α Receptor 1 Mediates Borna Disease Virus 1-Induced Changes in Peroxisomal and Mitochondrial Dynamics in Neurons.International journal of molecular sciences · 2024Article
- Necroptosis inhibition counteracts neurodegeneration, memory decline, and key hallmarks of aging, promoting brain rejuvenation.Aging cell · 2023Article
- Neurogenesis is disrupted in human hippocampal progenitor cells upon exposure to serum samples from hospitalized COVID-19 patients with neurological symptoms.Molecular psychiatry · 2022Article
- Microglia shield the murine brain from damage mediated by the cytokines IL-6 and IFN-α.Frontiers in immunology · 2022Article
- Glucocorticoid treatment of MCMV infected newborn mice attenuates CNS inflammation and limits deficits in cerebellar development.PLoS pathogens · 2013Article
- TNF-overexpression in Borna disease virus-infected mouse brains triggers inflammatory reaction and epileptic seizures.PloS one · 2012Article
- Opposing roles for CXCR3 signaling in central nervous system versus ocular inflammation mediated by the astrocyte-targeted production of IL-12.The American journal of pathology · 2011Article
- Transgenic models for cytokine-induced neurological disease.Biochimica et biophysica acta · 2010Review
- Trafficking of immune cells in the central nervous system.The Journal of clinical investigation · 2010Review
- Interferon-gamma prevents death of bystander neurons during CD8 T cell responses in the brain.The American journal of pathology · 2009Article
- Antiviral CD8 T cells recognize borna disease virus antigen transgenically expressed in either neurons or astrocytes.Journal of virology · 2008Article
- Downregulation of an astrocyte-derived inflammatory protein, S100B, reduces vascular inflammatory responses in brains persistently infected with Borna disease virus.Journal of virology · 2007Article
- Innate immune responses in NF-kappaB-repressing factor-deficient mice.Molecular and cellular biology · 2006Article
- CD8 T cells require gamma interferon to clear borna disease virus from the brain and prevent immune system-mediated neuronal damage.Journal of virology · 2005Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transgenic expression of interleukin-12 (IL-12) in astrocytes causes a spontaneous inflammatory central nervous system disorder in aged mice. Here we show that spontaneous disorder developed only when both mature lymphocytes and interferon (IFN)-gamma were present. Infection with noncytolytic Borna disease virus (BDV) did not affect wild-type mice but accelerated disease of IL-12 transgenic mice. Infection of transgenic mice lacking lymphocytes did not result in neurological symptoms. In contrast, BDV infection of transgenic mice lacking IFN-gamma induced neurological disease with delayed onset of symptoms that resembled those in infected transgenic mice with a functional IFN-gamma gene. In BDV-infected transgenic mice devoid of IFN-gamma no cerebellar calcification was observed, and multiplication of BDV was not inhibited. To determine the antigen specificity of lymphocytes in brains of diseased animals, the IL-12 transgene was introduced into an H-2k genetic background. Infection of IL-12 transgenic H-2k mice resulted in extensive lymphocytic infiltration into the cerebellum but not into other brain regions that also contained viral antigen but expressed the transgene at lower levels. Tetramer analysis revealed that most CD8 T cells in the cerebellum of such mice were BDV-specific. Our results thus demonstrate that IFN-gamma secreting lymphocytes are responsible for disease of IL-12 transgenic mice. They further suggest that expression of IL-12 in the central nervous system may lead to localized recruitment of T cells that recognize antigens expressed in the brain.
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