Multiple sclerosis is a disease characterized by demyelination of axons as well as chronic inflammation. Multiple sclerosis exists in several forms; the majority of patients show a relapsing and remitting type of disease. These patients experience demyelination and inflammation but this resolves after some time. This process occurs multiple times during the course of disease, with each subsequent relapse being slightly worse, until they finally progress to secondary progressive multiple sclerosis [108]. The observation that there is resolution suggests that M1/M2 dynamics might be relevant for this disease. Although the initial cause of inflammation is not clear, it has been observed that T cells, specifically Th1 and Th17 cells, are important contributors to multiple sclerosis pathology [109]. As previously stated, Th1 cell-secreted IFNγ is a potent inducer of M1 cells, suggesting during the active phase that microglia are skewed towards M1 activation. Although T cells regulate the response, microglia and macrophages are the effector cells. Several groups have begun to examine these dynamics in vivo using the multiple sclerosis animal model experimental autoimmune encephalitis (EAE).
