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首页> 外文期刊>Nature >Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination
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Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination

机译：共生菌群和髓磷脂自身抗原共同触发自身免疫性脱髓鞘

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摘要

Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter1. 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 infection2. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis3, 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 glyco-protein (MOG), and commensal microbiota. Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets.
机译：活动性多发性硬化病灶显示炎症变化，提示自身反应性T和B淋巴细胞对脑白质的联合攻击1。这些病原性免疫细胞源自祖细胞，这些祖细胞是健康免疫谱中的正常，无害成分，但在病理激活后会自激。触发这种自身免疫转化的刺激通常归因于环境因素，尤其是微生物感染2。但是，使用自发发展的实验性自身免疫性脑脊髓炎3的复发-缓解小鼠模型，在这里我们显示，在缺乏病原体的情况下，共鸣肠道菌群在触发免疫过程中是必不可少的，从而导致由髓磷脂驱动的复发-缓解性自身免疫疾病特异的CD4〜+ T细胞。我们进一步表明，从内源性免疫库中募集和激活自身抗体生产性B细胞取决于靶自身抗原，髓鞘少突胶质细胞糖蛋白（MOG）和共生菌群的可用性。我们的观察结果确定了触发器官特异性自身免疫性疾病的一系列事件，这些过程可能会提供新的治疗靶标。

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  • 来源
    《Nature》 |2011年第7374期|p.538-541|共4页
  • 作者

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

  • 作者单位

    Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany;

    Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany;

    Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany;

    Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany;

    Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany;

    Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg, Germany.;

    Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany;

    Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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