Central Laboratory, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan, China.
Neuroscience. 2013 Nov 12;252:320-5. doi: 10.1016/j.neuroscience.2013.08.025. Epub 2013 Aug 28.
Autism is a severe neurodevelopmental disorder characterized by impairments in social interaction, deficits in verbal and non-verbal communication, and repetitive behavior and restricted interests. Emerging evidence suggests that aberrant neuroimmune responses may contribute to phenotypic deficits and could be appropriate targets for pharmacologic intervention. Interleukin (IL)-6, one of the most important neuroimmune factors, has been shown to be involved in physiological brain development and in several neurological disorders. For instance, findings from postmortem and animal studies suggest that brain IL-6 is an important mediator of autism-like behaviors. In this review, a possible pathological mechanism behind autism is proposed, which suggests that IL-6 elevation in the brain, caused by the activated glia and/or maternal immune activation, could be an important inflammatory cytokine response involved in the mediation of autism-like behaviors through impairments of neuroanatomical structures and neuronal plasticity. Further studies to investigate whether IL-6 could be used for therapeutic interventions in autism would be of great significance.
自闭症是一种严重的神经发育障碍，其特征是社交互动受损、言语和非言语交流缺陷、重复行为和兴趣受限。新出现的证据表明，异常的神经免疫反应可能导致表型缺陷，并可能成为药物干预的适当靶点。白细胞介素 (IL)-6 是最重要的神经免疫因子之一，已被证明参与生理脑发育和多种神经疾病。例如，尸检和动物研究的结果表明，大脑中的 IL-6 是自闭症样行为的重要介质。在这篇综述中，提出了自闭症背后的一种可能的病理机制，即由于激活的神经胶质细胞和/或母体免疫激活导致大脑中 IL-6 升高，可能是通过损害神经解剖结构和神经元可塑性来介导自闭症样行为的重要炎症细胞因子反应。进一步研究 IL-6 是否可用于自闭症的治疗干预将具有重要意义。
