Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the CNS. Many findings support the assumption that the immune system plays a key role in the pathogenesis of MS, at least during the relapsing-remitting phase of disease.(1,2) Both arms of the adapted immune response seem to be crucial for the induction and maintenance of the autoimmune response as suggested by the success of therapies targeting T cells, B cells, or both. While genes and pathways involved in the pathogenesis of MS have emerged from recent studies, the molecular targets of the autoimmune response in MS are still largely uncertain. The identification of these targets, to better understand the pathogenesis and develop specific immune therapies, has been the focus of MS research during the last decades.