Westall Fred C
Institute for Disease Research, P.O. Box 890193, Temecula, CA 92589, USA.
J Clin Microbiol. 2006 Jun;44(6):2099-104. doi: 10.1128/JCM.02532-05.
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.
分子模拟是微生物感染产生自身免疫副作用的一种可能解释。将特定微生物的蛋白质序列与已知的自身免疫性免疫原进行比较。对于诸如多发性硬化症(MS)这类感染源未知的疾病,则对其病原体身份进行推测。一般认为模拟物很罕见。本研究采用了一种截然不同的方法。在所有已知的人类细菌和病毒病原体的报告序列中搜索自身免疫性免疫原模拟物。选择了三种已对其自身免疫性需求进行广泛研究的致脑炎肽进行比较。在各种各样的生物体中都发现了模拟物。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,因此有人提出,导致MS自身免疫活动的微生物可能是一种常见的肠道细菌。这将解释许多MS独特的流行病学数据,以及为何尚未确定MS的感染源,并支持最近发现的MS肠道代谢异常现象。