Department of Neurology, Northwestern University, Chicago, IL, USA.
J Parkinsons Dis. 2022;12(s1):S5-S11. doi: 10.3233/JPD-223240.
Accumulating evidence implicates immune dysfunction in the etiology of Parkinson's disease (PD). For instance, impaired cellular and humoral immune responses are emerging as established pathological hallmarks in PD. Further, in experimental models of PD, inflammatory cell activation and immune dysregulation are evident. Genetic and epidemiologic studies have drawn associations between autoimmune disease and PD. Distillation of these various lines of evidence indicates dysregulated immunogenetics as a primary risk factor for PD. This article will present novel perspectives on the association between genetic risk factors and immune processes in PD. The objective of this work is to synthesize the data surrounding the role of immunogenetics in PD to maximize the potential of targeting the immune system as a therapeutic modality.
越来越多的证据表明免疫功能障碍与帕金森病 (PD) 的病因有关。例如，细胞和体液免疫反应受损正在成为 PD 的既定病理标志。此外，在 PD 的实验模型中，炎症细胞激活和免疫失调是显而易见的。遗传和流行病学研究已经将自身免疫性疾病与 PD 联系起来。这些不同证据的提炼表明，免疫遗传学失调是 PD 的主要危险因素。本文将提出 PD 中遗传风险因素与免疫过程之间关联的新观点。这项工作的目的是综合围绕免疫遗传学在 PD 中的作用的数据，以最大限度地发挥将免疫系统作为治疗模式的潜力。
