Microglia, inflammasomes and multiple sclerosis (365E03417)
Multiple sclerosis (MS) is the most common chronic inflammatory disease of the central nervous system (CNS). MS is prevalent in Caucasians, where it affects about 0.1 % of the population (Trapp and Nave (2008) Annu Rev Neurosci 31, 247-269), which means for a country like Belgium that about 10.000 patients suffer from the disease. The cause of degeneration in MS remains largely enigmatic, but the disease is generally considered to be the result of an autoimmune inflammatory reaction characterized by activated auto-reactive myelin-specific lymphocytes that home to the CNS where they initiate a vicious cycle of inflammation, oligodendrocyte loss, demyelination, and axonal damage. The major targets in MS pathology are oligodendrocytes, the myelin-producing cells of the CNS, and neurons, and their loss is directly associated with clinical manifestations of the disease, including speech disturbances, sensation deficits and paralysis. Astrocytes and microglia, the other CNS resident cell types, are considered to act as effector cells during pathology, since more and more evidence indicates that both cell types actively contribute to the inflammatory reactions in MS (Dendrou et al. (2015) Nat Rev Immunol. 15, 545-558). An important experimental model to study the human disease is the model of Experimental Autoimmune Encephalomyelitis (EAE), which can be induced in rodents by immunization with myelinspecific antigens. Important knowledge concerning the molecular mechanisms driving MS pathology came from studies using this model (Baxter (2007) Nat Rev Immunol 7, 904-912).