Induction of a non-encephalitogenic type 2 T helper-cell autoimmune response in multiple sclerosis a

Author:  ["Ludwig Kappos","Giancarlo Comi","Hillel Panitch","Joel Oger","Jack Antel","Paul Conlon","Lawrence Steinman","Giancarlo Comi","Ludwig Kappos","Joel Oger","Hillel Panitch","Alexander Rae-Grant","John Castaldo","Nancy Eckert","Joseph B. Guarnaccia","Pamela Mills","Gary Johnson","Peter A. Calabresi","Carlo Pozzilli","Stefano Bastianello","Elisabetta Giugni","Tatiana Witjas","Patrick Cozzone","Jean Pelletier","Dieter Pöhlau","Horst Przuntek","Volker Hoffmann","Christopher Bever Jr","Eleanor Katz","Michel Clanet","Isabelle Berry","David Brassat","Irene Brunet","Gilles Edan","Pierre Duquette","Ernst-Wilhelm Radue","Dagmar Schött","Carmen Lienert","Alice Taksaoui","M. Rodegher","M. Filippi","Alan Evans","Pierre Bourgouin","Alex Zijdenbos","Shawki Salem","Nicholas Ling","David Alleva","Eric Johnson","Amitabh Gaur","Paul Crowe","Xin-Jun Liu"]

Publication:  Nature Medicine

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Tags:     Medicine

Abstract

In this ‘double-blind’, randomized, placebo-controlled phase II trial, we compared an altered peptide ligand of myelin basic protein with placebo, evaluating their safety and influence on magnetic resonance imaging in relapsing–remitting multiple sclerosis. A safety board suspended the trial because of hypersensitivity reactions in 9% of the patients. There were no increases in either clinical relapses or in new enhancing lesions in any patient, even those with hypersensitivity reactions. Secondary analysis of those patients completing the study showed that the volume and number of enhancing lesions were reduced at a dose of 5 mg. There was also a regulatory type 2 T helper-cell response to altered peptide ligand that cross-reacted with the native peptide.

Cite this article

Kappos, L., Comi, G., Panitch, H. et al. Induction of a non-encephalitogenic type 2 T helper-cell autoimmune response in multiple sclerosis after administration of an altered peptide ligand in a placebo-controlled, randomized phase II trial. Nat Med 6, 1176–1182 (2000). https://doi.org/10.1038/80525

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