Malashenkova I K, Krynskiy S A, Ogurtsov D P, Mamoshina M V, Zakharova N V, Ushakov V L, Velichkovsky B M, Didkovsky N A
Research Center 'Kurchatov Institute', Moscow, Russia; Federal Research and Clinical Center of Physical-Chemical Medicine, Moscow.
Research Center 'Kurchatov Institute', Moscow, Russia.
Zh Nevrol Psikhiatr Im S S Korsakova. 2018;118(12):72-80. doi: 10.17116/jnevro201811812172.
The review addresses immunological aspects of schizophrenia, a multifactor disease caused by genetic factors, innate disorders of the central nervous system (CNS), including the consequences of perinatal hypoxia and infections, and adverse environmental influences. Neuroinflammation as a part of the pathophysiology of schizophrenia is characterized by the higher transcription of CNS inflammatory mediators, excessive activation of microglia, inhibition of glutamatergic receptors that leads to the decrease in the number of cortical synapses and neuronal apoptosis. The authors discuss a role of genetic polymorphisms of cytokine genes, complement system components etc. The literature data on the changes in systemic immune response and imbalance in Th1/Th2 adaptive immune responses are analyzed as well. Some papers showed higher levels of proinflammatory mediators in CSF and blood of patients with schizophrenia that indicated the involvement of blood brain barrier (BBB) dysfunction. The authors present the recent data on BBB dysfunction in schizophrenia and its role in the pathogenesis of the disease, autoimmunity in patients comparing it with immune activation and genetic predisposition. An important and arguable issues about a role of parasite and viral infections in the pathogenesis of schizophrenia, initiation of immune responses and direct impacts on the brain, an influence of antipsychotic treatment on immunity are discussed. In author's opinion, conflicting results of genetic and immunological studies of schizophrenia may be explained by different methodological approaches to selection of patients and healthy controls and the differences in schizophrenia classification.
本综述探讨了精神分裂症的免疫学方面，这是一种由遗传因素、中枢神经系统（CNS）的先天性疾病（包括围产期缺氧和感染的后果）以及不良环境影响引起的多因素疾病。神经炎症作为精神分裂症病理生理学的一部分，其特征在于中枢神经系统炎症介质的转录增加、小胶质细胞的过度激活、谷氨酸能受体的抑制，这导致皮质突触数量减少和神经元凋亡。作者讨论了细胞因子基因、补体系统成分等的基因多态性的作用。还分析了关于全身免疫反应变化和Th1/Th2适应性免疫反应失衡的文献数据。一些论文显示，精神分裂症患者脑脊液和血液中的促炎介质水平较高，这表明血脑屏障（BBB）功能障碍的参与。作者介绍了精神分裂症中血脑屏障功能障碍的最新数据及其在疾病发病机制中的作用，将患者的自身免疫与免疫激活和遗传易感性进行了比较。讨论了关于寄生虫和病毒感染在精神分裂症发病机制中的作用、免疫反应的启动和对大脑的直接影响以及抗精神病治疗对免疫的影响等重要且有争议的问题。作者认为，精神分裂症遗传和免疫学研究结果相互矛盾，可能是由于患者和健康对照选择的方法不同以及精神分裂症分类的差异所致。
