Abstract
The relationship between immune responses to self-antigens and autoimmune disease is unclear. In contrast to its animal model experimental autoimmune encephalomyelitis (EAE), which is driven by T cell responses to myelin antigens, the target antigen of the intrathecal immune response in multiple sclerosis (MS) has not been identified. Although the immune response in MS contributes significantly to tissue destruction, the action of immunocompetent cells within the central nervous system (CNS) may also hold therapeutic potential. Thus, treatment of MS patients with glatiramer acetate triggers a protective immune response. Here we review the immunopathogenesis of MS and some recent findings on the mechanism of glatiramer acetate (GA).
Highlights
Autoimmunity can be defined as an adaptive immune response directed against the body’s own tissues
Most T and B cells carrying such self-reactive receptors are deleted during maturation, a high frequency of autoreactive T cells, B cells and autoantibodies is present in the normal repertoire without causing disease
Mononuclear infiltrates of CD4+ T and CD8+ T cells, B cells and macrophages are present to various extents and are thought to be critical for disease development and progression
Summary
Autoimmunity can be defined as an adaptive immune response directed against the body’s own tissues. At the beginning of the twentieth century, the German physician Paul Ehrlich coined the term “horror autotoxicus” arguing that the normal body would never mount an immune response against its own tissue. According to this view, any autoimmune reaction was destructive and connected to human disease. Most T and B cells carrying such self-reactive receptors are deleted during maturation, a high frequency of autoreactive T cells, B cells and autoantibodies is present in the normal repertoire without causing disease. It is proposed that recognition of self. Recognition of self-proteins in the absence of costimulation is important for the maintenance of immunological tolerance [5]
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