Immunopathogenic mechanisms in tourette syndrome: A critical review.
Immunopathogenic mechanisms in tourette syndrome: A critical review.
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DOI：
10.1002/mds.22504
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发表时间：
2009-07-15
影响因子：
8.6
通讯作者：
Leckman, James F.
中科院分区：
文献类型：
--
作者：
Martino, Davide;Dale, Russell C.;Gilbert, Donald L.;Giovannoni, Gavin;Leckman, James F.
抽动秽语综合征 (TS) 具有多因素病因，其中遗传、环境、免疫和激素因素相互作用，导致易感性。本综述：(i) 总结了探索 TS 患者暴露于免疫激活环境因素的研究，(ii) 重点关注支持先天性和适应性免疫系统在 TS 和相关疾病发病机制中的作用的最新研究结果。据记录，患有抽动症和强迫症 (OC) 症状的儿童在发病前暴露于 A 组 β-溶血性链球菌 (GABHS) 感染的情况较高，但它们对病程的影响仍不确定。外周免疫细胞基因表达谱、淋巴细胞亚群相对频率以及免疫效应分子合成的变化表明 TS 中免疫反应激活增加。控制自然杀伤和细胞毒性 T 细胞的基因表达增加、与疾病严重程度相关的一些促炎细胞因子的血浆水平增加以及抗神经元抗体的合成增加表明细胞介导机制的活性增加。重要的方法学差异可能导致针对 TS 自身抗体的研究结果之间存在一些不一致。最后，调节性 T 细胞频率的降低表明 TS 患者普遍易发生自身免疫反应，从而诱导对自身抗原的耐受。尽管免疫激活在 TS 中的致病作用尚未得到明确证实，但提出了一种病理生理学模型来解释免疫对多巴胺传递调节和抽动产生的可能影响。
Tourette syndrome (TS) has a multifactorial etiology, in which genetic, environmental, immunological and hormonal factors interact to establish vulnerability. This review: (i) summarizes research exploring the exposure of TS patients to immune-activating environmental factors, and (ii) focuses on recent findings supporting a role of the innate and adaptive immune systems in the pathogenesis of TS and related disorders. A higher exposure prior to disease onset to group A β-haemolytic streptococcal (GABHS) infections in children with tics and obsessive-compulsive (OC) symptoms has been documented, although their influence upon the course of disease remains uncertain. Increased activation of immune responses in TS is suggested by changes in gene expression profiles of peripheral immune cells, relative frequency of lymphocyte subpopulations, and synthesis of immune effector molecules. Increased activity of cell-mediated mechanisms is suggested by the increased expression of genes controlling natural killer and cytotoxic T cells, increased plasma levels of some pro-inflammatory cytokines which correlate with disease severity, and increased synthesis of antineuronal antibodies. Important methodological differences might account for some inconsistency among results of studies addressing autoantibodies in TS. Finally, a general predisposition to autoimmune responses in TS patients is indicated by the reduced frequency of regulatory T cells, which induce tolerance towards self-antigens. Although the pathogenic role of immune activation in TS has not been definitively proven, a pathophysiological model is proposed to explain the possible effect of immunity upon dopamine transmission regulation and the generation of tics.
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