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Nat Med. 2009 Jun;15(6):626-32. doi: 10.1038/nm.1975.

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

Author information

1
Department of Neuroimmunology, Max Planck Institute of Neurobiology, Martinsried, Germany.

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-Ab-restricted epitope sequences of MOG35-55 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 MOG35-55-I-Ab-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.

PMID:
19483694
DOI:
10.1038/nm.1975
[Indexed for MEDLINE]

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