[Multiple sclerosis: molecular and cellular mechanisms].

Multiple sclerosis (MS) is a chronic central nervous system disease of considerable medical and social impact. It is characterized by destruction of the myelin, the axon proteolipid sheath, or demyelination. While the etiology of MS remains unknown, one of the most well-grounded theories of its pathogenesis postulates that immunomediated inflammatory processes play the main role in myelin damage. The leading role in the autoimmune disturbance development belongs to T-cell system, however, B-cells also participate in the pathological process. Both genetical predisposition and environmental influence are involved in MS development. Correlations were found between MS and numerous environmental factors, including ecology and different infectious agents. However, no single environmental factor and no single infection was confirmed to be the primary cause of MS. The predisposition to MS seems to depend on several genes. Alleles and haplotypes of HLA genes which are the main human immune-response genes are undoubtedly associated with MS. Serological methods have shown weak association of MS with A3 and B7 loci of HLA class I. Stronger association was found for HLA class II haplotype specified to DR2(DR15), DQ6(DQ1) in serology typing nomenclature or DRB11501, DQA10102, DQB1*0602 in sequence-based genotyping terminology. Besides, MS was found to be associated with alleles of genes of T-cell receptors, cytokines, myelin components and some others, although these results are sometimes contradictory. The analysis of genetical predisposition factors and of possible mechanisms of their involvement in demyelination process on molecular and cellular levels should enlighten the MS pathogenesis and provide new ways of medical treatment and prevention of MS.