More MS news articles for May 2002

Multiple MAG peptides are recognized by circulating T and B lymphocytes in polyneuropathy and multiple sclerosis

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11985632&dopt=Abstract

Eur J Neurol 2002 May;9(3):243-251
Andersson M, Yu M, Soderstrom M, Weerth S, Baig S, Linington C, Solders G, Link H.
Department of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden, Department of Ophthalmology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden, Department of Neuroimmunology, Max-Planck Institute for Psychiatry, Martinsried, Germany, Section of Neurology, Department of Medicine, The Aga Khan University Hospital, Karachi, Pakistan.

Abnormal immune responses to myelin associated glycoprotein (MAG), a component of myelin of the central and peripheral nervous system, have been suggested to play a role in the pathogenesis of multiple sclerosis (MS) and certain types of inflammatory polyneuropathy

To identify possible immunodominant MAG peptides in neuroinflammation, we examined T and B cell responses to five selected synthetic MAG peptides and myelin proteins in 21 patients with non-inflammatory polyneuropathy, 26 patients with MS, 10 optic neuritis patients and 17 healthy subjects

Enzyme-linked immunosorbent spot-forming cell assays were adopted, allowing the detection and enumeration of individual antigen responsive T and B cells in body fluids

Patients with polyneuropathy as well as those with MS had elevated levels of T and B cells recognizing MAG and its peptides

Any of the five MAG peptides under study functioned as immunodominant T and/or B cell epitope in individual subjects

None of the MAG peptides elicited a specific disease-associated T or B cell response

The enhanced T and B cell response to myelin components like MAG may play some role in initiation and/or progression of these diseases, but they could also represent secondary responses associated with myelin damage and indicate tolerization rather than autoaggressive immunity.