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Myelin-specific T cells also recognize neuronal autoantigen in a transgenic mouse model of multiple sclerosis

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Krishnamoorthy,  G.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Domingues,  H. S.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Dornmair,  K.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Mentele,  R.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Kurschus,  F. C.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Wekerle,  H.
Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society;

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Citation

Krishnamoorthy, G., Saxena, A., Mars, L. T., Domingues, H. S., Ben-Nun, A., Lassmann, H., et al. (2009). Myelin-specific T cells also recognize neuronal autoantigen in a transgenic mouse model of multiple sclerosis. Nature Medicine, 15(6), 626-632.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-2079-E
Abstract
We describe here the paradoxical development of spontaneous experimental autoimmune encephalomyelitis (EAE) in transgenic mice expressing a myelin oligodendrocyte glycoprotein (MOG)-specific T cell antigen receptor (TCR) in the absence of MOG. We report that in Mog-deficient mice (Mog(-/-)), the autoimmune response by transgenic T cells is redirected to a neuronal cytoskeletal self antigen, neurofilament-M (NF-M). Although components of radically different protein classes, the cross-reacting major histocompatibility complex I-A(b)-restricted epitope sequences of MOG(35-55) and NF-M18-30 share essential TCR contact positions. This pattern of cross-reaction is not specific to the transgenic TCR but is also commonly seen in MOG(35-55)-I-A(b)-reactive T cells. We propose that in the C57BL/6 mouse, MOG and NF-M response components add up to overcome the general resistance of this strain to experimental induction of autoimmunity. Similar cumulative responses against more than one autoantigen may have a role in spontaneously developing human autoimmune diseases.