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首页> 外文期刊>Journal of Clinical Microbiology >Molecular Mimicry Revisited: Gut Bacteria and Multiple Sclerosis
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Molecular Mimicry Revisited: Gut Bacteria and Multiple Sclerosis

机译:再谈分子模拟:肠道细菌和多发性硬化症。

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Molecular mimicry is a possible explanation for autoimmune side effects of microorganism infections. Protein sequences from a particular microorganism are compared to known autoimmune immunogens. For diseases such as multiple sclerosis (MS), where the infectious agent is unknown, guesses to its identity are made. Mimics are assumed to be rare. This study takes a radically different approach. Reported sequences from all known human bacterial and viral agents were searched for autoimmune immunogen mimics. Three encephalitogenic peptides, whose autoimmune requirements have been studied extensively, were selected for comparison. Mimics were seen in a wide variety of organisms. For each immunogen, the mimics were found predominantly in nonpathogenic gut bacteria. Since the three immunogens used in this study are related to MS, it is suggested that a microorganism responsible for autoimmune activity in MS could be a normally occurring gut bacterium. This would explain many of the peculiar MS epidemiological data and why no infective agent has been identified for MS and supports recently found MS gut metabolism abnormalities.
机译:分子模拟是微生物感染自身免疫副作用的可能解释。将来自特定微生物的蛋白质序列与已知的自身免疫免疫原进行比较。对于未知传染原的多发性硬化症(MS)之类的疾病,要猜测其身份。模仿被认为是罕见的。这项研究采用了截然不同的方法。从所有已知的人类细菌和病毒制剂报告的序列中搜索自身免疫免疫原模拟物。选择了三种自身免疫要求已被广泛研究的脑致病肽进行比较。在各种各样的生物中都可以看到模拟物。对于每种免疫原,模拟物主要存在于非致病性肠道细菌中。由于本研究中使用的三种免疫原与MS相关,因此提示负责MS中自身免疫活性的微生物可能是正常的肠道细菌。这将解释许多特殊的MS流行病学数据,以及为什么没有为MS鉴定出感染因子并支持最近发现的MS肠道代谢异常的原因。

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