ABSTRACT

Multiple sclerosis (MS) is a chronic inflammatory, demyelinating disease of the central nervous system (CNS). Although the aetiology of MS is unknown, it is widely accepted that the disease is caused by a dysregulated T-cell response against brain resident antigens on the basis of a polygenic trait.1,2 However, predisposing genetic factors and immunological mechanisms leading to brain-specific chronic inflammation are largely unknown. One of the most appealing concepts for the development of MS is the ‘molecular mimicry’ hypothesis. It suggests that immunological cross-recognition of foreign and self-antigens is the key event for the induction of autoimmunity.