ausblenden:
Schlagwörter:
GRAY-MATTER ATROPHY; NEUROMYELITIS-OPTICA; ANTIBODIES; INJURY;
AUTOIMMUNITY; PATHOLOGY; ANTIGEN; DISEASE; MOGClinical Neurology; Neurosciences; Multiple sclerosis; Experimental autoimmune encephalomyelitis;
Autoantibodies; Myelin oligodendrocyte glycoprotein; Neurofascin;
Contactin-2;
Zusammenfassung:
Multiple sclerosis is a chronic inflammatory disease of the white and
grey matter which results in irrevocable axonal and neuronal damage.
Grey matter injury is widespread and reflects disability to a greater
extent than do white matter lesions. Growing understanding of the
immunopathology of multiple sclerosis is leading the way to the
identification and testing of untapped targets that may offer new and
more specific ways to treat the disease. For example, data from animal
models support a two-step pathological process in multiple sclerosis,
whereby T cells initially induce inflammation and open up the
blood-brain barrier, which then allows access to antibodies which
aggravate tissue damage. Determination of the specificity of the
invading T cells and the autoantibodies that cause disease is a major
focus of current research. The discovery of anti-aquaporin-4
autoantibodies in patients with neuromyelitis optica and of anti-MUG
antibodies in a subset of children with paediatric autoimmune
demyelinating disease are promising steps in this direction. Recently,
the axoglial antigens neurofascin and contactin-2/TAG-1, which are
localised around the node of Ranvier, were identified as targets of an
autoimmune response in multiple sclerosis. Such an autoimmune response
might induce axonal injury and direct the immunopathological response
to the grey matter. It is to be hoped that the outcome of such
investigations will lead to the identification of patient subgroups
based on their autoreactivity and new ways to treat them safely and
effectively. (C) 2011 Elsevier B.V. All rights reserved.
