Drug News Perspect. 2003 Nov; 16(9): 574-84Lyons JA.
Department of Health Sciences, University of Wisconsin, Milwaukee, Wisconsin, USA
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system characterized by the destruction of the myelin sheath surrounding axons.
On the basis of data from the animal model, experimental autoimmune encephalomyelitis (EAE) and the detection of myelin-reactive cells in MS patients, this destruction is thought to be due to an autoimmune T-cell-mediated response to myelin antigens.
Until recently, the characterization of T-cell recognition of myelin antigens has necessarily focused on the response to myelin proteins.
However, the discovery of CD1-mediated presentation of lipids and glycolipids to a variety of T-cell populations has greatly expanded the repertoire of antigens to which T cells can respond.
Studies in the EAE model suggest a role for myelin lipids in disease pathogenesis.
Recent characterization of the expression and function of CD1 and the responding T-cell populations does support a role for this pathway in the disease process.
Furthermore, data suggest that it may be possible to modulate the disease course by targeting this pathway.
Characterization of CD1-mediated presentation of lipids to T cells has only recently been investigated in MS, with most attention focusing on the expression of group I CD1 proteins in MS lesions.
In light of data from the animal model, further characterization of the expression and function of group I and group II CD1 proteins is warranted, and could lead to the development of effective therapies to treat MS.