ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
CD8+ lymphocyte-mediated injury of dorsal root ganglion neurons during lentivirus infection: CD154-dependent cell contact neurotoxicity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
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- T cells at the interface of neuroimmune communication.The Journal of allergy and clinical immunology · 2024Review
- Cytotoxic Immunity in Peripheral Nerve Injury and Pain.Frontiers in neuroscience · 2020Review
- Applications of the FIV Model to Study HIV Pathogenesis.Viruses · 2018Review
- Animal models of HIV peripheral neuropathy.Future virology · 2014Article
- Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Animal models of peripheral neuropathies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2012Review
- Proteinase-activated receptor-1 mediates dorsal root ganglion neuronal degeneration in HIV/AIDS.Brain : a journal of neurology · 2011Article
- Neurologic presentations of AIDS.Neurologic clinics · 2010Review
- Evidence for predilection of macrophage infiltration patterns in the deeper midline and mesial temporal structures of the brain uniquely in patients with HIV-associated dementia.BMC infectious diseases · 2009Article
- CD8+ T cells directed against a viral peptide contribute to loss of motor function by disrupting axonal transport in a viral model of fulminant demyelination.Journal of neuroimmunology · 2007Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal damage in dorsal root ganglia (DRGs) with accompanying axonal injury is a key feature of human immunodeficiency virus (HIV)-related distal sensory polyneuropathy (DSP). In a model of HIV-related DSP, we observed numerous CD3+ T lymphocytes (p < 0.05) in DRGs from feline immunodeficiency virus (FIV)-infected animals, which also exhibited low CD4+ and high CD8+ lymphocyte levels in blood accompanied by a selective loss of small-diameter sural nerve axons (p < 0.05). FIV-infected lymphocytes cocultured with syngeneic DRGs caused neuronal damage, indicated by neurite retraction, neuronal soma atrophy, and loss (p < 0.05). In contrast, supernatants from FIV-infected or uninfected lymphocytes were minimally neurotoxic, despite high FIV virion levels. Among lymphocyte subsets cocultured with DRG cultures, CD8+ T cells from both FIV-infected and uninfected lymphocytes selectively caused DRG neuronal injury (p < 0.05). FIV-infected CD8+ T cells showed markedly increased CD154 expression (p < 0.05), whereas neurons were the predominant cells expressing CD40 in DRGs. Blocking CD154 on activated CD8+ T cells protected DRG neurons (p < 0.05). These findings indicated that CD8+ T cells were principal effectors of DRG neuronal injury after FIV infection through a CD40-CD154 interaction in a cell contact-dependent manner.
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