ABSTRACT
Multiple sclerosis (MS) is considered a T-cellmediated inflammatory demyelinating disease of the central nervous system (CNS) with various degrees of axonal loss.1-5 While its aetiology remains unknown, evidence from various sources, including wellstudied animal models, i.e. experimental allergic encephalomyelitis (EAE), and the characterization of human myelin-specific T cells support a role of autoreactive T cells in disease pathogenesis.6,7 It is now clear that a number of myelin and glial components can serve as target antigens in the encephalitogenic process and induce different forms of EAE. Based on these exciting findings in animal models, human myelin-specific T cells have been studied in great detail during the last decade. There are many parallels between those cells that can transfer disease in the animal model and T cells that have been isolated from MS patients, i.e. they are CD4+ T-helper (Th) cells that frequently express a proinflammatory phenotype, so-called T-helper 1 cells (Th1) based on their secretion of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α).6,8-10 With our growing understanding of the molecular aspects of immune function in general and the activation requirements, phenotype and effector functions of T cells in particu lar, there is a strong interest to translate this knowledge into specific immune interventions. These will eventually target individual aspects of the inflammatory demyelinating disease. One would hope that they will lead to effective inhibition of the autoimmune process, without compromising the patient’s immune system and without invoking as many adverse reactions as the currently used immunomodulatory treatments.
