[Intercellular adhesion molecules and chemotaxic factors in the pathogenesis of multiple sclerosis]

Multiple sclerosis (MS) is an inflammatory immune disorder of the central nervous system characterized by the destruction of myelin sheaths and the cells which make them, the oligodendrocytes. Experimental allergic encephalitis (EAE) is an autoimmune condition mainly induced by the myelin basic protein (MBP) that is a very useful model for the study of demyelinating inflammatory diseases, particularly MS.

Cellular adhesion molecules are a wide group of membrane receptors which mediate adhesion processes, both cell to cell and between cells and the extracellular matrix. These molecules play an essential role in inflammatory phenomena, including EAE/MS. Integrins of the b1 subfamily (mainly a4b1), as well as leukocyte integrins and adhesion receptors of the immunoglobulin superfamily (ICAM 1, VCAM 1) are the main molecules involved. Chemokines also have an important role in MS, since they are able to attract and activate leukocytes, essential phenomena in the inflammatory reaction. An increased expression of chemokines CC or beta (e.g., RANTES, MIP 1a and b, MCP 1, etc.) has been found in EAE/MS, and it is very likely that they are involved in the migration of lymphocytes and monocytes towards the MS inflammatory lesions.

The pharmacological blockade of adhesion molecules and chemokines is a promising and novel therapeutic approach in MS.