Gendelman Howard E
J Neurovirol. 2002 Dec;8(6):474-9. doi: 10.1080/13550280290168631.
The articles compiled in this special edition of Journal of NeuroVirology target a developing field of investigation seeking to uncover how the immune system affects both the pathogenic process and protection against the ravages of neurodegenerative processes. Whether caused by a microbe, trauma, toxic metabolite, autoimmunity, or part of a wide degenerative process, immune dysfunction commonly affects central nervous system (CNS) disease. All together, the work presented here proved to be a unique undertaking with contributing scientists outside the field of neurovirology. Indeed, multiple disciplines including molecular neuroscience, neuroimmunology, virology, cellular immunology, receptor pharmacology, neuronal electrophysiology, neurochemistry, clinical neurology, and development neurobiology were joined. The basis of this work rests with the hypothesis that brain mononuclear phagocytes (MP; perivascular and brain macrophages and microglia) act as inducers of disease by engaging the immune system to protect, defend, or induce neural injury. Indeed, it is the brain MP that act as scavengers killing microblial pathogens, regulate immune responses through antigen presentation and mobilization of adaptive immune activities, and affect the production of neurotrophic or toxic secretory factors that incite disease processes. For many years, these responses were thought to be reactive to ongoing disease mechanisms with little effects on disease itself, let alone repair. The works compiled in this issue demonstrate quite clearly this is no longer true. Immune responses cannot be directed only against a microbe but also against self-antigens that are expressed in damaged CNS, leading to innate neurotoxic or adaptive anti-self immunity that commonly follow viral infections. Importantly, therapeutic modalities may take advantage of CNS immune responses through vaccination generating neuroprotection. Together, these articles serve to bring together common neuroimmune links between highly divergent diseases (for example, Parkinson's and Alzheimer's disease and human immunodeficiency virus type-one dementia). In the end, I hope this work will serve as discussion points for future collaborations and began to break down the barriers of disease, enabling targeted research activities toward what we have in common.
《神经病毒学杂志》本期特刊汇编的文章聚焦于一个正在发展的研究领域，该领域旨在揭示免疫系统如何影响致病过程以及对神经退行性病变的抵御作用。无论是由微生物、创伤、毒性代谢产物、自身免疫，还是广泛的退行性病变过程的一部分引起，免疫功能障碍通常都会影响中枢神经系统（CNS）疾病。总体而言，这里呈现的工作被证明是一项独特的事业，参与的科学家来自神经病毒学领域之外。实际上，多个学科包括分子神经科学、神经免疫学、病毒学、细胞免疫学、受体药理学、神经元电生理学、神经化学、临床神经学和发育神经生物学都参与其中。这项工作的基础基于这样一个假设，即脑单核吞噬细胞（MP；血管周围巨噬细胞、脑巨噬细胞和小胶质细胞）通过激活免疫系统来保护、防御或诱导神经损伤，从而成为疾病的诱导因素。的确，正是脑MP作为清除剂杀死微生物病原体，通过抗原呈递和适应性免疫活动的动员来调节免疫反应，并影响促发疾病过程的神经营养或毒性分泌因子的产生。多年来，这些反应被认为是对正在进行的疾病机制的反应，对疾病本身影响甚微，更不用说修复了。本期汇编的作品清楚地表明情况已不再如此。免疫反应不仅可以针对微生物，还可以针对受损中枢神经系统中表达的自身抗原，导致通常在病毒感染后出现的先天性神经毒性或适应性自身免疫。重要的是，治疗方式可以通过疫苗接种产生神经保护作用来利用中枢神经系统的免疫反应。总之，这些文章有助于汇集高度不同疾病（例如帕金森病、阿尔茨海默病和人类免疫缺陷病毒1型痴呆）之间常见的神经免疫联系。最后，我希望这项工作将成为未来合作的讨论要点，并开始打破疾病的障碍，使有针对性的研究活动朝着我们的共同之处开展。
