Neuron
ArticleNeuronal cells are deficient in loading peptides onto MHC class I molecules
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2022, Trends in NeurosciencesCitation Excerpt :While the specificity of CNS-infiltrating cytotoxic lymphocytes (CTLs) has not been determined in many different neurodegenerative diseases, several studies have focused instead on the targets of these cells. Healthy neurons typically express very little MHC I [79,80] but can sometimes upregulate antigen-presenting machinery when distressed or following changes in neural activity [81,82]. Aberrant protein accumulation in neurons during neurodegenerative diseases has the potential to enhance the expression of antigen-presenting molecules like β2-microglobulin and MHC I.
Immunological defense of CNS barriers against infections
2022, ImmunityCitation Excerpt :The T cell effector molecules IFNγ, tumor necrosis factor α (TNFα), and perforin all participate in controlling the virus; however, direct T cell engagement of infected cells is not required (Moseman et al., 2020). Within the CNS parenchyma, VSV is known to primarily infect neurons, although most neurons minimize T cell engagement because they display relatively low levels of peptide MHC I on their cell surface (Joly and Oldstone, 1992; Moseman et al., 2020). In addition, genetic removal of MHC I expression from VSV-infected cells in vivo has no impact on viral control (Moseman et al., 2020).
What Kaplan-Meier survival curves don't tell us about CNS disease
2017, Journal of NeuroimmunologyCitation Excerpt :Subsequent studies showed that this is not universally true: while the homeostatic expression of MHC class I is lower in neurons in general, neurons can up-regulate MHC class I under inflammatory conditions, thus making them susceptible to cytotoxic T cell attack (Neumann et al., 1997; Cebrián et al., 2014; Neumann et al., 1995). This could be virus- or strain-specific however, as others have reported little to no detectable MHC expression on neurons following infection with noncytolytic viruses, such as lymphocytic choriomeningitis virus, which might contribute to the ability of these viruses to establish persistent infections (Joly et al., 1991; Joly and Oldstone, 1992; Horwitz et al., 1999). Interestingly, clearance and control of many neuronal viral infections, while dependent on T cell receptor-MHC interaction, occurs in a non-cytolytic manner (Burdeinick-Kerr et al., 2009; Patterson et al., 2002; Griffin, 2010).
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Present address: ICRF, Clare Hall Laboratories, South Mimms, Potters Bar, Herts EN6 3LD, England.