Scott Kirsten M, Kouli Antonina, Yeoh Su L, Clatworthy Menna R, Williams-Gray Caroline H
Department of Clinical Neurosciences, John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, United Kingdom.
University of Cambridge School of Clinical Medicine, Cambridge, United Kingdom.
Front Neurol. 2018 Oct 1;9:815. doi: 10.3389/fneur.2018.00815. eCollection 2018.
Immune dysfunction has been associated with Parkinson's disease (PD) and its progression. Antibodies play an important role in both innate and adaptive responses, acting as powerful effector molecules that can propagate inflammation by activating innate immune cells. Alpha synuclein binding antibodies have been described in PD patients with conflicting associations. In this article, we consider the potential mechanistic basis of alpha synuclein auto-antibody development and function in PD. We present a systematic review and meta-analysis of antibody studies in PD cohorts showing that there is weak evidence for an increase in alpha synuclein auto-antibodies in PD patients particularly in early disease. The confidence with which this conclusion can be drawn is limited by the heterogeneity of the clinical cohorts used, inclusion of unmatched controls, inadequate power and assay related variability. We have therefore made some recommendations for the design of future studies.
免疫功能障碍与帕金森病（PD）及其进展有关。抗体在先天性和适应性免疫反应中均发挥重要作用，作为强大的效应分子，可通过激活先天性免疫细胞来传播炎症。在帕金森病患者中，已报道了α-突触核蛋白结合抗体，但相关关联存在矛盾。在本文中，我们探讨了α-突触核蛋白自身抗体在帕金森病中产生和发挥作用的潜在机制基础。我们对帕金森病队列中的抗体研究进行了系统综述和荟萃分析，结果表明，几乎没有证据表明帕金森病患者尤其是早期患者体内α-突触核蛋白自身抗体增加。得出这一结论的可信度受到所用临床队列的异质性、未匹配对照的纳入、检验效能不足以及检测相关变异性的限制。因此，我们对未来研究的设计提出了一些建议。
