The concept of molecular mimicry describes situations in which antigen sharing between parasites and hosts could benefit pathogen evasion from host immune responses. However, antigen sharing can generate host responses to parasite-derived self-like peptides, triggering autoimmunity. Since its conception, molecular mimicry and the consequent potential cross-reactivity following infections have been repeatedly described in humans, raising increasing interest among immunologists. Here, we reviewed this concept focusing on the challenge of maintaining host immune tolerance to self-components in parasitic diseases. We focused on the studies that used genomics and bioinformatics to estimate the extent of antigen sharing between proteomes of different organisms. In addition, we comparatively analyzed human and murine proteomes for peptide sharing with proteomes of pathogenic and non-pathogenic organisms. We conclude that, although the amount of antigenic sharing between hosts and both pathogenic and non-pathogenic parasites and bacteria is massive, the degree of this antigen sharing is not related to pathogenicity or virulence. In addition, because the development of autoimmunity in response to infections by microorganisms endowed with cross-reacting antigens is rare, we conclude that molecular mimicry by itself is not a sufficient factor to disrupt intact self-tolerance mechanisms.

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再次考察分子拟态：致病性、毒力和自身免疫

分子拟态的概念描述了寄生虫和宿主之间抗原共享可以有利于病原体逃避宿主免疫反应的情况。然而，抗原共享可以产生宿主对寄生虫衍生的自样肽的反应，从而引发自身免疫。自其概念诞生以来，分子拟态及其感染后潜在的交叉反应已在人类中被反复描述，引起了免疫学家越来越多的兴趣。在这里，我们回顾了这一概念，重点关注维持宿主对寄生虫病自身成分的免疫耐受性的挑战。我们专注于使用基因组学和生物信息学来估计不同生物体蛋白质组之间抗原共享程度的研究。此外，我们比较分析了人类和小鼠蛋白质组与致病性和非致病性生物体蛋白质组的肽共享。我们的结论是，尽管宿主与致病性和非致病性寄生虫和细菌之间的抗原共享量很大，但这种抗原共享的程度与致病性或毒力无关。此外，由于具有交叉反应抗原的微生物感染而产生自身免疫的情况很少见，因此我们得出结论，分子拟态本身不足以破坏完整的自我耐受机制。这种抗原共享的程度与致病性或毒力无关。此外，由于具有交叉反应抗原的微生物感染而产生自身免疫的情况很少见，因此我们得出结论，分子拟态本身不足以破坏完整的自我耐受机制。这种抗原共享的程度与致病性或毒力无关。此外，由于具有交叉反应抗原的微生物感染而产生自身免疫的情况很少见，因此我们得出结论，分子拟态本身不足以破坏完整的自我耐受机制。