内生
免疫学
肿瘤坏死因子α
病态行为
温度调节
设定值
免疫系统
白细胞介素
解热药
促炎细胞因子
下丘脑
细胞因子
医学
炎症
生物
神经科学
内分泌学
药理学
控制工程
工程类
止痛药
作者
Matthew J. Kluger,Wiesław Kozak,Lisa R. Leon,Dariusz Soszyński,Carole A. Conn
摘要
Fever is an excellent example of neuroimmunomodulation in that mediators of immunity initiate a pathway to raise the thermoregulatory set-point, resulting in behavioral and physiological responses that increase body temperature. This rise in temperature is thought to be adaptive, facilitating host defenses. Many cytokines are endogenous mediators of fever (i.e. endogenous pyrogens), including interleukin (IL)-, 1 beta, IL-6 and others. Tumor necrosis factor-alpha may be both an endogenous pyrogen and an endogenous antipyretic or cryogen, depending on the nature of the inflammatory stimuli. Although there is evidence that cytokines within the hypothalamus initiate fever, recent findings indicate that the signal to increase these brain cytokines may be neural (i.e. from peripheral nerves), rather than humoral (i.e. circulating endogenous pyrogen).
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