Abstract
Myelin oligodendrocyte glycoprotein (MOG) is the only myelin protein known to initiate a demyelinating autoantibody response in EAE, an animal model for multiple sclerosis (MS). The pathophysiological significance of MOG-specific autoantibodies in MS is, however, controversial, as high titer antibody responses to MOG are also found in many patients with non-demyelinating neurological diseases. In this issue of the European Journal of Immunology, von Budingen et al. demonstrate that demyelination in a primate model of MOG-induced EAE is mediated by MOG-specific antibodies directed against discontinuous, rather than linear, MOG epitopes. This functional segregation of pathogenic vs. non-pathogenic autoantibodies in terms of epitope specificity may be crucial to understand the relevance of MOG-specific responses in human disease. This commentary discusses these findings in the context of the structure and immunobiology of MOG, and their implications with respect to antibody-mediated demyelination in MS.
Original language | English |
---|---|
Pages (from-to) | 2065-2071 |
Number of pages | 6 |
Journal | European Journal of Immunology |
Volume | 34 |
Issue number | 8 |
DOIs | |
Publication status | Published - 2004 |
Keywords
- B cells
- demyelination
- multiple sclerosis
- experimental autoimmune encephalomyelitis
- EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS
- EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
- MULTIPLE-SCLEROSIS PATHOLOGY
- ANTIGEN-SPECIFIC ANTIBODY
- B-CELL RESPONSES
- MOG-INDUCED EAE
- MYELIN/OLIGODENDROCYTE GLYCOPROTEIN
- BASIC-PROTEIN
- T-CELL
- MONOCLONAL-ANTIBODY