• tumour necrosis factor
• central nervous system
• demyelinating disease

Multiple sclerosis is a primary demyelinating disease in which an inflammatory cell infiltrate represents a characteristic pathological feature of active lesions within the central nervous system (CNS). As the search for anti-myelin antibodies in multiple sclerosis has thus far been unsuccessful, the possibility is raised that cell mediated immune mechanisms orchestrate the pathogenesis of this disease.1 In cellular immune mechanisms cytokines play a particularly important part. Tumour necrosis factors (TNFs) form a unique family of cytokines that are very pleiotropic in nature.2 TNFs demonstrate immunoregulatory activity but they are also involved in the effector arm of cellular immune responses. TNF increases antigen and mitogen induced T lymphocyte activation,3 as well as increasing the generation of cytotoxic T cells.4 Studies both in vitro and in vivo have suggested a role for TNFs in the pathology of multiple sclerosis. In this report, I will summarise data for and against involvement of TNFs in the mechanisms of multiple sclerosis and attempt to apply an anti-TNF approach for future therapeutic strategy for this disease.