Multiple sclerosis

Abstract

Multiple sclerosis (MS) is an inflammatory disease characterized by demyelination and axonal degeneration in the central nervous system (CNS). Although MS is considered an autoimmune disease against myelin antigens, its pathogenesis still remains unclear. Microglia are macrophage-like cells in the CNS which play a critical role in innate immunity, in addition to activating pathways associated with adaptive immunity. Microglia produce pro-inflammatory and anti-inflammatory mediators, including cytokines and chemokines, and phagocytose various types of cellular debris. In MS, microglia critically contribute to the inflammatory milieu, but also participate in disrupting the blood-brain barrier integrity, thus inducing the migration of various types of immune cells such as T and B lymphocytes, macrophages, and neutrophils into the CNS. In this disease, microglia may additionally behave as antigen-presenting cells and function as effector cells causing demyelination and axonal degeneration. However, recent evidence also indicates that microglia could play a beneficial role in remyelination and neuroprotection in MS. In this chapter, we will discuss about microglial involvement in MS, with an emphasis on the experimental autoimmune encephalomyelitis (EAE) animal model and describe the cellular and molecular mechanisms which could be specifically implicated in the pathogenesis.