Aboul-Enein F, Lassmann H
Center for Brain Research, Medical University of Vienna, Austria.
Acta Neuropathol. 2005 Jan;109(1):49-55. doi: 10.1007/s00401-004-0954-8. Epub 2005 Jan 11.
The immunological mechanisms leading to tissue damage in inflammatory brain diseases are heterogeneous and complex. They may involve direct cytotoxicity of T lymphocytes, specific antibodies and activated effector cells, such as macrophages and microglia. Here we describe that in certain inflammatory brain lesions a pattern of tissue injury is present, which closely reflects that found in hypoxic conditions of the central nervous system. Certain inflammatory mediators, in particular reactive oxygen and nitrogen species, are able to mediate mitochondrial dysfunction, and we suggest that these inflammatory mediators, when excessively liberated, can result in a state of histotoxic hypoxia. This mechanism may play a major role in multiple sclerosis, not only explaining the lesions formed in a subtype of patients with acute and relapsing course, but also being involved in the formation of diffuse "neurodegenerative" lesions in chronic progressive forms of the disease.
导致炎症性脑部疾病组织损伤的免疫机制是异质性且复杂的。它们可能涉及T淋巴细胞的直接细胞毒性、特异性抗体以及活化的效应细胞，如巨噬细胞和小胶质细胞。在此我们描述，在某些炎症性脑损伤中存在一种组织损伤模式，这与中枢神经系统缺氧状态下发现的模式密切相关。某些炎症介质，特别是活性氧和氮物种，能够介导线粒体功能障碍，并且我们认为这些炎症介质在过度释放时可导致组织中毒性缺氧状态。这种机制可能在多发性硬化症中起主要作用，不仅可以解释急性和复发型患者亚型中形成的病变，还参与了该疾病慢性进展型中弥漫性“神经退行性”病变的形成。
