Schuld A, Hinze-Selch D, Pollmächer Th
Max-Planck-Institut für Psychiatrie München, Germany.
Nervenarzt. 2004 Mar;75(3):215-26. doi: 10.1007/s00115-003-1599-x.
Experimental findings from psychoimmunologic research in humans and epidemiological data suggest that alterations in cytokine networks may induce acute psychopathologic symptoms and may be involved in the pathogenesis and pathophysiology of schizophrenia by influencing brain development. However, there is insufficient evidence from genetic, post-mortem, and cerebrospinal fluid studies to demonstrate this in the CNS of schizophrenic patients. In contrast, there are quite robust findings from peripheral blood that interleukin (IL)-2, IL-6, tumor necrosis factor-alpha, and interferon cytokine systems in patients are regulated differently than in controls. However, these findings are not specific to schizophrenia, they are confounded by numerous intervening variables such as stress, smoking, and medication, and their pathophysiologic relevance for processes in the CNS is undetermined. Therefore, future research on the involvement of cytokines in the pathogenetics, pathophysiology, and treatment of schizophrenia is needed.
来自人类心理免疫学研究的实验结果和流行病学数据表明,细胞因子网络的改变可能诱发急性精神病理症状,并可能通过影响大脑发育参与精神分裂症的发病机制和病理生理学过程。然而,来自遗传学、尸检和脑脊液研究的证据不足,无法在精神分裂症患者的中枢神经系统中证实这一点。相比之下,外周血有相当确凿的发现,即患者体内的白细胞介素(IL)-2、IL-6、肿瘤坏死因子-α和干扰素细胞因子系统与对照组的调节方式不同。然而,这些发现并非精神分裂症所特有,它们受到压力、吸烟和药物治疗等众多干预变量的混淆,其对中枢神经系统过程的病理生理学相关性尚未确定。因此,需要对细胞因子参与精神分裂症的发病机制、病理生理学和治疗进行进一步研究。