[疟原虫和格林-巴利综合征抗原之间的分子模拟]。

Yuliana Marcela Emiliani-Navarro, D Vega, G Muzi, Marlon Munera-Gomez, Andrés Sánchez
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引用次数: 0

摘要

目的分析疟原虫与 GBS 相关自身抗原之间的分子拟态,确定可能的抗原表位:方法:使用 PSI-Blast、Praline、Emboss、Protein Data Bank、Swiss Model Server、AlphaFold 2、Ellipro 和 PyMol 2.3 搜索同源性、进行比对、获取蛋白质结构并预测表位:结果:共纳入了 17 个自身抗原和 7 个外周神经系统免疫靶标,确定了 72 个可能与 GBS 相关的表位。在疟原虫蛋白质组(298个蛋白质)中,只有两个蛋白质与TRIM21和BACE1的相似度接近30%,从而产生了7个可能的表位:建议探讨其他机制,如免疫介导的毛细血管损伤、表位扩散或旁观者激活,以解释上述关联。这些发现强调了阐明自身免疫性疾病病因和病原体作用的必要性。强调需要进行实验研究来验证这些结果。
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[Molecular mimicry between Plasmodium sp and Guillain-Barre syndrome antigens].

Objective: Analyze the molecular mimicry between Plasmodium spp. and autoantigens associated with GBS, identifying possible antigenic epitopes.

Methods: PSI-Blast, Praline, Emboss, Protein Data Bank, Swiss Model Server, AlphaFold 2, Ellipro and PyMol 2.3 were used to search for homologies, perform alignments, obtain protein structures, and predict epitopes.

Results: 17 autoantigens and seven immunological targets of the peripheral nervous system were included, identifying 72 possible epitopes associated with GBS. From the proteome of Plasmodium spp. (298 proteins), only two showed similarities close to 30% with TRIM21 and BACE1, generating seven possible epitopes.

Conclusion: No significant homologies were observed between the proteome of GBS and Plasmodium spp. The exploration of other mechanisms such as immune-mediated capillary damage, Epitope Spreading or Bystander Activation is suggested to explain the mentioned association. These findings underscore the need to clarify the etiology of autoimmune diseases and the role of pathogens. The need for experimental studies to validate these results is emphasized.

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