Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination

Kerstin Berer, Marsilius Mues, Michail Koutrolos, Zakeya Al Rasbi, Marina Boziki, Caroline Johner, Hartmut Wekerle () and Gurumoorthy Krishnamoorthy ()
Additional contact information
Kerstin Berer: Max Planck Institute of Neurobiology, 82152 Martinsried, Germany
Marsilius Mues: Max Planck Institute of Neurobiology, 82152 Martinsried, Germany
Michail Koutrolos: Max Planck Institute of Neurobiology, 82152 Martinsried, Germany
Zakeya Al Rasbi: Max Planck Institute of Neurobiology, 82152 Martinsried, Germany
Marina Boziki: Max Planck Institute of Neurobiology, 82152 Martinsried, Germany
Caroline Johner: Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany
Hartmut Wekerle: Max Planck Institute of Neurobiology, 82152 Martinsried, Germany
Gurumoorthy Krishnamoorthy: Max Planck Institute of Neurobiology, 82152 Martinsried, Germany

Nature, 2011, vol. 479, issue 7374, 538-541

Abstract: Role of gut bacteria in triggering multiple sclerosis There is controversy over the nature of the early stages of multiple sclerosis: some suggest that the initiation process involves primary changes in the central nervous system, others that pathogenesis originates in the immune system. Support for the latter concept comes from the finding that intact commensal microbiota are required for autoimmune disease in a spontaneous mouse model for relapsing–remitting multiple sclerosis. Microbial exposure is necessary but not sufficient for disease induction, which requires the presence of the target myelin autoantigen, MOG. The possible involvement of diet and microbiota in autoimmune disease may provide novel therapeutic approaches.

Date: 2011
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DOI: 10.1038/nature10554

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