Prion-like behaviour is an abrupt process, an “all-or-nothing” transition between a monomeric species and an “infinite” fibrillated form. Once a nucleation point is formed, the process is unstoppable as fibrils self-propagate by recruiting and converting all monomers into the amyloid fold. After the “mad cow” episode, prion diseases have made the headlines, but more and more prion-like behaviours have emerged in neurodegenerative diseases, where formation of fibrils and large conglomerates of proteins deeply disrupt the cell homeostasis. More interestingly, in the last decade, examples emerged to suggest that prion-like conversion can be used as a positive gain of function, for memory storage or structural scaffolding. More recent experiments show that we are only seeing the tip of the iceberg and that, for example, prion-like amplification is found in many pathways of the immune response. In innate immunity, receptors on the cellular surface or within the cells ‘sense’ danger and propagate this information as signal, through protein-protein interactions (PPIs) between ‘receptor’, ‘adaptor’ and ‘effector’ proteins. In innate immunity, the smallest signal of a foreign element or pathogen needs to trigger a macroscopic signal output, and it was found that adaptor polymerize to create an extreme signal amplification. Interestingly, our body uses multiple structural motifs to create large signalling platform; a few innate proteins use amyloid scaffolds but most of the polymers discovered are composed by self-assembly in helical filaments. Some of these helical assemblies even have intercellular “contamination” in a “true” prion action, as demonstrated for ASC specks and MyD88 filaments. Here, we will describe the current knowledge in neurodegenerative diseases and innate immunity and show how these two very different fields can cross-seed discoveries.

类病毒的行为是一个突然的过程，是单体物种与“无限”原纤维化形式之间的“全有或全无”过渡。一旦形成成核点，该过程就无法停止，因为通过募集所有单体并将其转化为淀粉样蛋白折叠，从而使原纤维自蔓延。在“疯牛病”事件之后，病毒疾病成为头条新闻，但在神经退行性疾病中出现了越来越多的病毒样行为，其中原纤维的形成和蛋白质的大团聚严重破坏了细胞的体内平衡。更有趣的是，在过去的十年中，出现了一些实例表明，病毒样的转化可以用作功能性的正向获得，用于记忆存储或结构性脚手架。最近的实验表明，我们只看到冰山一角，例如，在免疫反应的许多途径中都发现了ion病毒样的扩增。在先天免疫中，细胞表面或细胞内的受体会“感知”危险，并通过“受体”，“衔接子”和“效应子”蛋白之间的蛋白质-蛋白质相互作用（PPI）将这些信息作为信号传播。在先天免疫中，外来元素或病原体的最小信号需要触发宏观信号输出，并且发现衔接子聚合以产生极端的信号放大。有趣的是，我们的身体使用多种结构图案来创建大型信号平台。少数先天蛋白使用淀粉样蛋白支架，但发现的大多数聚合物是由螺旋丝中的自组装组成的。其中一些螺旋装配甚至在“真正的” pr病毒作用中具有细胞间“污染”，如ASC斑点和MyD88细丝所示。在这里，我们将描述有关神经退行性疾病和先天免疫的最新知识，并展示这两个截然不同的领域如何跨种子发现。