Journal
NATURE MEDICINE
Volume 15, Issue 6, Pages 626-U142Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.1975
Keywords
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Funding
- Deutsche Forschungsgemeinschaft (Sonderforschungsbereiche (SFB) 571
- Max Planck Society
- Portuguese Fundacao para a Ciencia ea Tecnologia (FCT) [SFRH/BD/15885/2005]
- EU Project Neuropromise [PL 018637]
- Israel Science Foundation
- National Multiple Sclerosis Society of New York [RG3195B8/2]
- Alexander von Humboldt Prize Awardee
- Fundação para a Ciência e a Tecnologia [SFRH/BD/15885/2005] Funding Source: FCT
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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.
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