No human protein is exempt from bacterial motifs, not even one.

Brett Trost, Guglielmo Lucchese, Angela Stufano, Mik Bickis, Anthony Kusalik, Darja Kanduc
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引用次数: 75

Abstract

The hypothesis that mimicry between a self and a microbial peptide antigen is strictly related to autoimmune pathology remains a debated concept in autoimmunity research. Clear evidence for a causal link between molecular mimicry and autoimmunity is still lacking. In recent studies we have demonstrated that viruses and bacteria share amino acid sequences with the human proteome at such a high extent that the molecular mimicry hypothesis becomes questionable as a causal factor in autoimmunity. Expanding upon our analysis, here we detail the bacterial peptide overlapping to the human proteome at the penta-, hexa-, hepta- and octapeptide levels by exact peptide matching analysis and demonstrate that there does not exist a single human protein that does not harbor a bacterial pentapeptide or hexapeptide motif. This finding suggests that molecular mimicry between a self and a microbial peptide antigen cannot be assumed as a basis for autoimmune pathologies. Moreover, the data are discussed in relation to the microbial immune escape phenomenon and the possible vaccine-related autoimmune effects.

Abstract Image

Abstract Image

没有一种人类蛋白质可以不受细菌基序的影响,甚至一个都不能。
自我与微生物肽抗原之间的模仿与自身免疫病理密切相关的假设在自身免疫研究中仍然是一个有争议的概念。分子模仿与自身免疫之间的因果关系尚缺乏明确的证据。在最近的研究中,我们已经证明病毒和细菌与人类蛋白质组在如此高的程度上共享氨基酸序列,以至于分子模仿假说作为自身免疫的因果因素受到质疑。在我们的分析基础上,我们通过精确的肽匹配分析,详细描述了细菌肽与人类蛋白质组在五、六、七和八肽水平上的重叠,并证明不存在不包含细菌五肽或六肽基序的单一人类蛋白质。这一发现表明,自身和微生物肽抗原之间的分子模仿不能被认为是自身免疫病理的基础。此外,这些数据还讨论了微生物免疫逃逸现象和可能的疫苗相关自身免疫效应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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