Hunt Nicholas H, Grau Georges E
Department of Pathology, D06, University of Sydney, Sydney, NSW 2006, Australia.
Trends Immunol. 2003 Sep;24(9):491-9. doi: 10.1016/s1471-4906(03)00229-1.
Cerebral malaria (CM) is a major life-threatening complication of Plasmodium falciparum infection. The nature of the pathogenetic processes leading to the cerebral complications is poorly understood. Mouse models of this condition have provided insight into the key events in pathogenesis, including those that occur before clinical symptoms are seen. Some T helper 1 (Th1) cytokines (e.g. interferon-gamma, lymphotoxin and tumour necrosis factor) have been implicated in driving the immunopathological process leading to CM, whereas some Th2 cytokines (e.g. interleukin-10, transforming growth factor-beta) appear to oppose this process. Upregulation of leukocyte adhesion molecules on the cerebral microvascular endothelium appears to be an important component of the proinflammatory actions of the cytokines. Activation of platelets in the cerebral microcirculation could also be a key event in CM. Furthermore, recent evidence has emerged indicating that cytokines might influence biochemical pathways in the brain that, in turn, could determine the outcome of CM.
脑型疟疾（CM）是恶性疟原虫感染的一种主要的危及生命的并发症。导致脑部并发症的发病机制的本质尚不清楚。这种病症的小鼠模型为发病机制中的关键事件提供了见解，包括那些在出现临床症状之前发生的事件。一些辅助性T细胞1（Th1）细胞因子（如干扰素-γ、淋巴毒素和肿瘤坏死因子）被认为在驱动导致脑型疟疾的免疫病理过程中起作用，而一些Th2细胞因子（如白细胞介素-10、转化生长因子-β）似乎对这一过程起对抗作用。脑微血管内皮细胞上白细胞粘附分子的上调似乎是细胞因子促炎作用的一个重要组成部分。脑微循环中血小板的激活也可能是脑型疟疾的一个关键事件。此外，最近有证据表明，细胞因子可能会影响大脑中的生化途径，进而可能决定脑型疟疾的结局。
