Abstract
In multiple sclerosis (MS), disability occurs as a result of complex interactions between glial cells and diverse components of acquired immunity. Microglial cells significantly contribute to disability progression by re-activating infiltrating lymphocytes, releasing neuro- and oligodendrocytotoxic mediators, inducing oxidative stress, and interfering with neuroplasticity. Recent research has emphasized the significance of meningeal B cell infiltrates in development of cognitive decline and disability. B cells are also involved in disability progression by way of production of neurotoxic antibodies directed against axoglial antigens. Among several immunological factors, neurofilament light chain antibodies, IgM-type oligoclonal bands, complement factor C3, and microglia-derived mediators stick out as potential reliable predictors of disability progression in MS patients. Better understanding of the interactions between innate immunity and neuroaxonal degeneration may result in development of novel and effective therapeutics for progressive types of MS.