As part of the innate immune system, complement plays a critical role in the elimination of pathogens and mobilization of cellular immune responses. In the central nervous system (CNS), many complement proteins are locally produced and regulate nervous system development and physiological processes such as neural plasticity. However, aberrant complement activation has been implicated in neurodegeneration, including Alzheimer's disease. There is a growing list of pathogens that have been shown to interact with the complement system in the brain but the short- and long-term consequences of infection-induced complement activation for neuronal functioning are largely elusive. Available evidence suggests that the infection-induced complement activation could be protective or harmful, depending on the context. Here we summarize how various infectious agents, including bacteria (e.g. Streptococcus spp.), viruses (e.g. HIV and measles virus), fungi (e.g. Candida spp.), parasites (e.g. Toxoplasma gondii and Plasmodium spp.), and prion proteins activate and manipulate the complement system in the CNS. We also discuss the potential mechanisms by which the interaction between the infectious agents and the complement system can play a role in neurodegeneration and dementia.

中文翻译：

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补体系统与传染原之间的相互作用——与神经退行性变和痴呆的潜在机制联系


作为先天免疫系统的一部分，补体在消除病原体和动员细胞免疫反应方面发挥着关键作用。在中枢神经系统（CNS）中，许多补体蛋白是局部产生的，调节神经系统发育和神经可塑性等生理过程。然而，异常的补体激活与神经变性有关，包括阿尔茨海默病。越来越多的病原体已被证明与大脑中的补体系统相互作用，但感染诱导的补体激活对神经元功能的短期和长期影响在很大程度上是难以捉摸的。现有证据表明，感染诱导的补体激活可能是保护性的，也可能是有害的，具体取决于具体情况。在这里，我们总结了各种感染因子，包括细菌（例如链球菌属）、病毒（例如艾滋病毒和麻疹病毒）、真菌（例如念珠菌属）、寄生虫（例如弓形虫和疟原虫属）和朊病毒蛋白如何激活和激活操纵中枢神经系统的补体系统。我们还讨论了感染因子和补体系统之间的相互作用在神经变性和痴呆中发挥作用的潜在机制。