https://jneuroinflammation.biomedcentra ... 017-1049-5
It is debated whether multiple sclerosis (MS) might result from an immunopathological response toward an active Epstein-Barr virus (EBV) infection brought into the central nervous system (CNS) by immigrating B cells. Based on this model, a relationship should exist between the local immune milieu and EBV infection status in the MS brain. To test this hypothesis, we analyzed expression of viral and cellular genes in brain-infiltrating immune cells.
These results confirm profound in situ EBV deregulation and suggest orchestration of local antiviral function in the MS brain, lending support to a model of MS pathogenesis that involves EBV as possible antigenic stimulus of the persistent immune response in the central nervous system.
"It is also known that the CNS immune infiltrate is dominated by CD8+ T cells displaying signs of local activation, like clonal expansion and expression of cytolytic enzymes. Both MS lesion analysis and experimental studies have highlighted a key role for CD8+ T cells in neurodegeneration [23, 24]. Recent studies point to a pathogenic role for granulocyte-macrophage colony-stimulating factor (GM-CSF) producing T cells in MS via enhanced myeloid cell recruitment and activation [25, 26], and GM-CSF producing CD4+ and CD8+ T cells have been identified in MS brain lesions"
"It has been suggested that Th17 cells may be implicated in the formation of ectopic lymphoid-like tissue in the inflamed CNS [32, 33]. Recently, clonally expanded CD4+ and CD8+ T cells with type 2 immunity functional features were identified in WM lesions characterized by complement and immunoglobulin deposition (pattern II brain lesions)"
Given that CD8+ T cells indicate EBV infection, I would say that pattern II MS is more clearly related to EBV than the other patterns.
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