Abstract
Current options for treatment of diseases with a presumed autoimmune etiology such as multiple sclerosis (MS) are far from satisfactory. Most treatments are associated with undesirable side effects due to toxicity and lack of immunological specificity. For these reasons, one of the primary goals in the development of immunotherapies has been to achieve selective inactivation of disease-inducing lymphocytes in the absence of general immunosuppression. It appears that the peripheral immune system can be divided into two compartments: one in which positive responses are initiated and another one where tolerance is induced (Mitchison 1998). Augmenting of tolerance by immunoregulation ranks prominently among the various approaches studied for the treatment of autoimmune disorders. Strategies in this direction include induction of specific immunological tolerance via anergizing, deletion, or suppression of autoreactive clones (Van Paris et al. 1998). The role of some of these mechanisms in maintaining peripheral tolerance in vivo is still very much a matter of debate.
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