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  Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination

Berer, K., Mues, M., Koutrolos, M., Al Rasbi, Z., Boziki, M., Johner, C., et al. (2011). Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination. NATURE, 479(7374), 538-541. doi:10.1038/nature10554.

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 Creators:
Berer, Kerstin1, Author              
Mues, Marsilius1, Author              
Koutrolos, Michail1, Author              
Al Rasbi, Zakeya1, Author              
Boziki, Marina1, Author              
Johner, Caroline2, Author
Wekerle, Hartmut1, Author              
Krishnamoorthy, Gurumoorthy1, Author              
Affiliations:
1Department: Neuroimmunology / Wekerle, MPI of Neurobiology, Max Planck Society, ou_1113547              
2External Organizations, ou_persistent22              

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Free keywords: T-CELL RESPONSES; MULTIPLE-SCLEROSIS; B-CELLS; TRANSGENIC MICE; AUTOANTIBODIES; INDUCTION; BACTERIA; DISEASE; MOG
 Abstract: Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter(1). These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection(2). However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis(3), here we show that the commensal gut flora-in the absence of pathogenic agents-is essential in triggering immune processes, leading to a relapsing-remitting autoimmune disease driven by myelin-specific CD4(+) T cells. We show further that recruitment and activation of autoantibody-producing B cells from the endogenous immune repertoire depends on availability of the target autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal microbiota. Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets.

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Language(s): eng - English
 Dates: 2011-11-24
 Publication Status: Published in print
 Pages: 5
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: ISI: 000297285600053
DOI: 10.1038/nature10554
 Degree: -

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Title: NATURE
Source Genre: Journal
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Publ. Info: MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND : NATURE PUBLISHING GROUP
Pages: - Volume / Issue: 479 (7374) Sequence Number: - Start / End Page: 538 - 541 Identifier: ISSN: 0028-0836