Gut microbiota from multiple sclerosis patients enables spontaneous autoimmune encephalomyelitis in mice
Kerstin Berer(Max Planck Institute of Neurobiology), Lisa Ann Gerdes, Egle Cekanaviciute(University of California, San Francisco), Xiaoming Jia(University of California, San Francisco), Liang Xiao(BGI Group (China)), Zhongkui Xia(BGI Group (China)), Chuan Liu(BGI Group (China)), Luisa Klotz(University Hospital Münster), Uta Stauffer(Max Planck Institute of Immunobiology and Epigenetics), Sergio E. Baranzini(University of California, San Francisco), Tania Kümpfel, Reinhard Hohlfeld(Munich Cluster for Systems Neurology), Gurumoorthy Krishnamoorthy(Max Planck Institute of Neurobiology), Hartmut Wekerle(Munich Cluster for Systems Neurology)
Cited by 933Open Access
Abstract
, an organism shown to induce a protective immunoregulatory profile in vitro. Immune cells from mouse recipients of MS-twin samples produced less IL-10 than immune cells from mice colonized with healthy-twin samples. IL-10 may have a regulatory role in spontaneous CNS autoimmunity, as neutralization of the cytokine in mice colonized with healthy-twin fecal samples increased disease incidence. These findings provide evidence that MS-derived microbiota contain factors that precipitate an MS-like autoimmune disease in a transgenic mouse model. They hence encourage the detailed search for protective and pathogenic microbial components in human MS.
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