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Pathophysiology of multiple sclerosis

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Abstract

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Both genetic and environmental causes for MS have been suggested. Recent genome-wide association studies revealed new susceptibility alleles for MS besides the HLA complex that are all related with immune functions. Whereas there is little evidence to support a purely environmental trigger for the disease in the sense of an infectious agent, the autoimmune hypothesis of MS is well established. Myelin antigen-specific CD4+ T cells become activated in the peripheral immune compartment, cross the blood-brain barrier and trigger the disease. Here, current concepts of the commitment of T cells to pro-inflammatory effector T helper cell lineages including Th17 cells that appear to be important inducers of organ-specific autoimmunity will be discussed.

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Correspondence to Thomas Korn.

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Conflict of interest The author declares no conflict of interest.

Acknowledgment T. Korn is supported by the Deutsche Forschungsgemeinschaft.

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Korn, T. Pathophysiology of multiple sclerosis. J Neurol 255 (Suppl 6), 2–6 (2008). https://doi.org/10.1007/s00415-008-6001-2

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  • DOI: https://doi.org/10.1007/s00415-008-6001-2

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