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¹ Department of Neuroimmunology and ² Transgenic Service, Max Planck Institute of Neurobiology, D-82152 Martinsried, Germany
³ Center for Brain Research, Medical University of Vienna, A-1090 Vienna, Austria
⁴ Department of Immunology, Biogen Idec, San Diego, CA 92122

CORRESPONDENCE Hartmut Wekerle: hwekerle{at}neuro.mpg.de OR Florian C. Kurschus: kurschus{at}neuro.mpg.de

We describe new T cell receptor (TCR) transgenic mice (relapsing-remitting [RR] mice) carrying a TCR specific for myelin oligodendrocyte glycoprotein (MOG) peptide 92–106 in the context of I-A^s. Backcrossed to the SJL/J background, most RR mice spontaneously develop RR experimental autoimmune encephalomyelitis (EAE) with episodes often altering between different central nervous system tissues like the cerebellum, optic nerve, and spinal cord. Development of spontaneous EAE depends on the presence of an intact B cell compartment and on the expression of MOG autoantigen. There is no spontaneous EAE development in B cell–depleted mice or in transgenic mice lacking MOG. Transgenic T cells seem to expand MOG autoreactive B cells from the endogenous repertoire. The expanded autoreactive B cells produce autoantibodies binding to a conformational epitope on the native MOG protein while ignoring the T cell target peptide. The secreted autoantibodies are pathogenic, enhancing demyelinating EAE episodes. RR mice constitute the first spontaneous animal model for the most common form of multiple sclerosis (MS), RR MS.

B. Pllinger's present address is Novartis Pharma AG, CH-4056 Basel, Switzerland.

F.C. Kurschus's present address is I. Medizinische Klinik und Poliklinik, Johannes Gutenberg Universität, D-55131 Mainz, Germany.

Abbreviations used: cDNA, complementary DNA; CNS, central nervous system; EAE, experimental autoimmune encephalomyelitis; MOG, myelin oligodendrocyte glycoprotein; MS, multiple sclerosis; NTL, nontransgenic littermate; OSE, opticospinal EAE; OSMS, opticospinal MS; PI, propidium iodide; rMOG, recombinant rat MOG; RR, relapsing-remitting.

© 2009 Pöllinger et al.
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