Encephalitogenic potential of the myelin basic protein peptide (amino acids 83–99) in multiple sclerosis: Results of a phase II clinical trial with an altered peptide ligand

By B. Bielekova, B. Goodwin, N. Richert, I. Cortese, T. Kondo, G. Afshar, B. Gran, J. Eaton, J. Antel, J. Frank and 2 more. Nature Medicine, 2000

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Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS) (2011, background): “Patients recovered well, and the therapeutic disappointment was at least partly compensated for by the scientific insight into the ability of modified MBP peptides to induce exacerbations in patients, thus confirming a long suspected link between autoimmunity to MBP and MS (Bielekova et al., 2000).”
Immunology of multiple sclerosis. (2005, methodology): “Furthermore, during a trial with an APL peptide derived from MBP(83−99), we identified TCC responding to both the APL peptide and MBP(83−99) at subnanomolar concentrations (101), and one of these TCC was present in the peripheral blood already seven years before the APL trial (107).”
Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. (2006, background): “The subsequent sophisticated attempts to modulate the antigen by creating altered peptide ligand (APL) and bring them to human therapy (Bielekova et al., 2000; Kappos et al., 2000) came to the surprising finding that the APLs were able to stimulate autoreactivity in some patients, while they dampen…”