Update on Inflammation, Neurodegeneration, and Immunoregulation in Multiple Sclerosis: Therapeutic Implications

Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system of uncertain etiology There is consensus that a dysregulated immune system plays a critical role in the pathogenesis of MS; therefore, we aim to summarize Current hypotheses concerning the complex cellular and molecular interactions involved in the immunopathology of MS. Although CD4(+) T lymphocytes have long been implicated in file immunopathology of MS, the role of other T-cell subtypes has been recognized. CD4(+) and CD8(+) cells have been isolated from different locations within MS lesions and gamma/delta T cells have been isolated from early MS lesions. The prevalent dogma has been that CD4(+) T(H)1 cells release cytokines and mediators of inflammation that may cause tissue damage, although CD4(+) T(H)2 cells may be involved in modulation of these effects. Recent evidence, however, suggests that additional T-cell subsets play a prominent role in MS immunopathology: T(H)17 cells, CD8(+) effector T cells, and CD4(+) CD25(+) regulatory T cells. In addition, laboratory and clinical data are accumulating oil the prominent role of B lymphocytes and antigen-presenting cells in MS pathogenesis, On the basis of these observations, new therapeutic approaches for MS will need to focus oil resetting multiple components of the immune system.