Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disorder of the CNS. The etiology of MS remains unknown. However, it is well established that immune dysregulation plays a critical role in the neuropathogenesis of this disorder. In this review, we discuss the current hypotheses concerning the complex cellular and molecular interactions involved in the immunopathogenesis of MS. Although CD4+ T lymphocytes have long been considered the critical cellular factor in the immunopathology of MS, the role of other cell types has also recently been investigated. It appears that the spatial distribution ofCD4+ andCD8+ cells inMS lesions is distinct. Yet another T-lymphocyte subset, γ/ε T cells, can be detected in very early MS lesions. The prevalent dogma suggests that CD4+ helper T (TH) type 1 cells release cytokines and inflammatory mediators that cause tissue damage, while CD4+ TH2 cells might be involved inmodulation of these effects.However, amounting body of evidence suggests that additional T-cell subsets, including TH17 cells,CD8+ effector T cells, and CD4+ CD25+ regulatory T cells, also affect disease activity. In addition, clinical and paraclinical data are accumulating on the prominent role of B lymphocytes and other antigen-presenting cells in MS neuropathogenesis. Given these observations, new therapeutic interventions for MS will need to focus on resetting multiple components of the immune system.
|Original language||English (US)|
|Number of pages||15|
|Journal||CONTINUUM Lifelong Learning in Neurology|
|State||Published - Oct 1 2010|
ASJC Scopus subject areas
- Clinical Neurology