Format

Send to

Choose Destination
J Neurol. 2008 Dec;255 Suppl 6:2-6. doi: 10.1007/s00415-008-6001-2.

Pathophysiology of multiple sclerosis.

Author information

1
Technische Universität München, Klinikum rechts der Isar, Department of Neurology, Ismaninger Str. 22, 81675 München, Germany. korn@lrz.tum.de

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.

PMID:
19300953
DOI:
10.1007/s00415-008-6001-2
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center