Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2011-11

AUTHORS

Kerstin Berer, Marsilius Mues, Michail Koutrolos, Zakeya Al Rasbi, Marina Boziki, Caroline Johner, Hartmut Wekerle, Gurumoorthy Krishnamoorthy

ABSTRACT

Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. 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. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, 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. More... »

PAGES

538

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature10554

DOI

http://dx.doi.org/10.1038/nature10554

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041793242

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22031325


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