Abstract: | Multiple sclerosis (MS) arises from T cell-mediated destruction of the myelin sheath. In MS patients who express the human leukocyte antigen (HLA)-DR2 haplotype (about two-thirds of MS patients), the major T cell response is directed to a region between residues 85 and 99 of myelin basic protein (MBP85 – 99) presented on HLA-DR2. One approved medication for MS, amino acid copolymer-1 (Cop-1, CopaxoneTM, Teva) is thought to alter this anti-MBP85 – 99 response by interacting with HLA-DR2, but is only partially effective. Here, synthetic peptides were designed according to the binding motif of MBP85 – 99 and the binding pockets of HLA-DR2. It is claimed that some of these peptides, which bind to HLA-DR2 and inhibit activation of MBP-specific T cell lines better than Cop-1, might be more effective than the latter for MS therapy. |